© Distribution of this video is restricted by its owner
Transcript ×
Auto highlight
Font-size
00:01 This is, yeah, I feel it. So, yeah.

00:30 folks. Uh welcome. Yeah. Today we are to remember we uh

00:42 you for last week, right? , uh we'll continue on um

00:53 what we're doing now is not a three coming up for sure.

00:58 um do you have any last minute ? You wanna stop by uh free

01:03 do that? So, um but so we are a little bit ahead

01:09 schedule and um I'll so remember, , I've taken it off of

01:15 but it still shows up on the . So this was written as a

01:20 class, but it's not OK. have it here for chapter 25 and

01:26 put that video up on uh today you can have access to that if

01:33 want that. Um And uh so uh will get, we'll finish 23

01:41 is the system, then we'll um at the beginning of 24 very early

01:47 and then continue that through um next . Ok. The uh so this

01:54 , aside from the exam three is weekly quiz, uh just covers the

02:00 system stuff if there's that many But, uh, anyway, we'll

02:05 through next, uh, um, through Monday as usual for that.

02:11 , um, so let's talk a bit. Well, let's do a

02:18 first. Ok. And then we'll of frame it around this question.

02:22 kind of, uh, um, think we talked about last time

02:29 Ok, so let me put uh, oh yeah, I

02:35 Let's see. Mobile responses start. we go. Ok. You get

02:42 . Yeah. So 4 33 Ok. So we talked about,

02:49 , these last time. So we're at these are all so all innate

03:00 system defenses. Oh, is types continue that. So they were kind

03:11 start talking about cell type. So go in the middle of that and

03:14 into some of the processes like, , uh, inflammatory response,

03:21 complement activation, some of these other . Ok. All right. Let's

03:53 this thing down here. Yeah. ticks left. Here we go.

04:30 . Yeah. The false one is , ok. Um, so as

04:36 said, these are all innate system . Let's kind of just recap a

04:41 bit from last time. So we of set this up and this

04:46 we'll talk about this, um, , certainly in chapter 25 next

04:52 Uh, and, uh, so setting this up as a, our

04:58 , right? Immune defenses we're focusing right now that the immune defenses.

05:05 , what are they, for most fight off obviously potential paths,

05:10 So there's a of the faction, ? They have a source, they

05:16 it to us in some form of , um then convert various factors,

05:21 ? Um In different parts of the from getting into you, staying around

05:26 you multiplying, et cetera. So we have look at it,

05:34 different lines of the fence if you . OK. So we have uh

05:39 line, second line you just always about, OK. What are

05:42 you know, here's a path coming the layers it has to get through

05:46 , right? So obviously a a physical barrier in the skin

05:52 right? Because not every the most that you um take in as far

05:57 an infection, breathing, breathe in in foodborne illness, drinking, contaminated

06:03 or other. Um These are all pass through mucus membrane or across along

06:09 membranes, right? Um The what else? Probably either through natural

06:16 in the skin, right? sweat glands or um or through a

06:22 look, right? Um And so um but don't ever forget these guys

06:29 , right? They're normal microbiota, ? So I remember that concept of

06:35 uh microbial antagonism, right? So microbes are very well adapted to your

06:42 and the various environments they inhabit in body and for something just to come

06:47 and, and crowd them out and over. It's not gonna be an

06:50 task, right. So it's a thing, you've got those there to

06:54 you. And then, uh we a little bit about uh types of

06:59 , not so much their functions right. These types here and we'll

07:04 more into what I call, I , these kind of processes.

07:09 but nonetheless, uh so one of main things here, we think of

07:14 mas, they also sometimes called tamp they're the same thing. OK.

07:20 the uh the fire, right, war going on here. And so

07:27 recognize uh is um of molecules on pathogens, right? Be it a

07:36 , be it a viral envelope protein what have you and then at least

07:42 cytokine cytokine, we heard more about today, really the context of inflammation

07:47 how that works. Uh But it's it's through chemicals, how you talk

07:51 your cells and bo by bonding to and then producing an effect. Um

07:57 so the these to like receptors, there's also the what they're called N

08:03 R S. And so the differentiation these uh external, right, internal

08:10 of these as uh external and internal . So they, they can buy

08:16 something and it's in, in, a sense as being something, you

08:20 that or something not good if you , but then it'll set the motion

08:26 of cytokines which have varied effects. four written here and a lot

08:33 OK. But it's how you get body mobilized to start doing stuff.

08:38 so cell types. So we went kind of the basics of cell

08:44 We'll focus more on that today. particularly in the context of phagocytosis,

08:52 ? That's one of the major infection is to them. OK?

09:03 the main ones are neutrophils, And uh macrophages for sure. And

09:10 a degree dendritic cells, those are three main ones, right? The

09:15 do this as well, but you when you call. So,

09:28 all right. So I think we off, we ended with these guys

09:32 , natural killer cells. OK. one of the things to remember is

09:38 pathogens come in various forms, You kind of break them down into

09:44 camps. How does that carry out whole infection process while outside of your

09:52 ? Right? Extra sata patterns, one in um they at some point

10:01 their infection cycle, get inside Viruses obviously do this, that's what

10:07 do. OK? But again, bactero types that do this too for

10:12 purpose, not of replicating in but that's for the purpose of hiding

10:16 and for penetrating deeper into your body you will see. OK. So

10:22 have to have defenses that work on types and something is inside the

10:27 It's someone invisible, right? That immune system cells can't see it.

10:33 not, it's the sound of one your cells. So there, but

10:36 ways to, to find those acts OK, what we call a defense

10:42 infected cells? Ok. So that is the natural killer cells is

10:49 of those? Ok. Um So do you find something that's infected?

10:56 inside. How do you know it's ? How is your immune system

11:02 Because in some, not in all , but in some cases, in

11:09 cases, um, changes occurred in surface because of the infection due to

11:17 infection changes occur and molecules on the or maybe some, some are missing

11:21 are normally there. That's what these look for. OK. Those are

11:27 , right? And that's something that , oh, this may be infected

11:30 . Let's get rid of it. ? And so what natural kill cells

11:34 for are the lack of the absence a reduction in these? OK.

11:44 I didn't even wanna go into that the end last time because N H

11:48 is A is a topic unto OK. So before we get into

11:54 , what they do to the cells basically um here you see a natural

11:58 cell um attacking an infected cell, ? Could be virus infected, it

12:04 be some other infected uh infection. And so Perris think of these as

12:12 little protein straws, right? Hollow the middle, they insert themselves into

12:18 membrane contents, leak out, kills , right? They also can produce

12:23 . Uh apoptosis is another way to rid of infected cells. Uh

12:28 other cell types do this as Ok. Um And so apoptosis,

12:35 typically, you hear it as a cell death, right? Your cells

12:39 this naturally. Ok? When they're the end of their life cycle.

12:44 . It can also be induced. sure many of us at sunburns.

12:50 . And so you, your skin red, it peels and it peels

12:53 , right? Those are your body rid of those, you know,

12:56 been bombarded with U V light, potentially mutated, potentially dangerous,

13:02 So your body kills them off right a poc through the. So

13:07 it's a natural process but can be by certain chemicals, you know,

13:14 certain circumstances. And one of them of course to get rid of the

13:17 , right? So you kill get out of the population, we

13:21 want you. Ok. So, to MC. So, um,

13:28 , um, let's just go flip here. Ok. So this

13:34 so if you have an immune system trying to, that's constantly on the

13:40 , let's say for cells that shouldn't in your body, right?

13:47 ok. Um, there has to a system that they can recognize,

13:53 ? You belong here, you don't terms. OK? That's what MH

14:00 molecules are all about. So you on your cells, these glyco

14:08 OK? That think of it as bar code, right? It's a

14:14 of amino acids, right? Um on your cells through sugar moles and

14:23 . And so that identifies your cells yours. Um When one gets

14:31 if one needs a organ transplant or transplant, what, what have you

14:37 these kind of things? We have uh put together tissues from different

14:43 Yeah. What one looks at are , what is the, what are

14:48 MH C molecules? What's the profile that look like between donor and

14:53 Right? Are they very similar? if they're not very similar, even

14:59 they are quite similar, you may have a reaction, right? Your

15:03 system will respond to it. I it's not yours. I'm gonna attack

15:08 . That's what tissue typing matching is about is making sure it's as close

15:12 possible. You don't want the, recipient to produce a response to,

15:18 , to kill the, the incoming . So uh in a way

15:23 so that's kind of what this is . OK. So again, you

15:26 your MH C bar codes and all cells. OK. So if something

15:31 coming in your body that's not it immediately knows. All right,

15:35 gotta do something. OK? And different immune system cells that respond to

15:40 . OK. Uh One of them talk about maybe, maybe later uh

15:46 or one of those that respond to . OK. Um OK. So

15:52 just like a very generic example of cell and it has it MH C

15:56 on it. OK. Could be of your cells. Now, the

16:01 , right? The easiest way is , to, to see what makes

16:05 class two in class one and class . So if you're a MH C

16:09 two cell, you're a B you're a macro, you're a dendritic

16:15 . OK? Um Anything else a one? Right? So all of

16:23 skin cells, your liver cells, brain cells, your intestinal cells,

16:29 cells of a part of your, your tissues here. These are all

16:33 one. OK. And so and we use the term nucleating,

16:39 So we have this similar self system red blood cells, right? So

16:49 B CS, right? When is antigen system? You know that what's

16:58 blood type? I know who the time is? Oh, that's

17:04 that's your blood, the A B system, that's for the red blood

17:08 . Same principle. OK. You that because if you have a certain

17:12 of blood, if you're a type and you get a type B,

17:17 it be a problem? Right? you may attack it. Your immune

17:20 thinks, oh, they don't have right antigens, right? They're not

17:24 right ones. So the A B system is your blood red blood

17:28 OK. This system is for everything . OK. So um OK.

17:36 remember M ac class two macrophages, cells and B cells. OK.

17:44 so that's what collectively we call these presenting cells. OK. Um We'll

17:51 that some of that in the context innate immune system because macrophages and dic

17:58 are, are a type that can in the immune system, they can

18:02 out with the system. We see . OK. So, um so

18:11 I mentioned, um the cell and men move into chapter 24 we'll talk

18:18 cells and B cells, but we it here just to kind of begin

18:22 about it. So, um and t cell interactions can create different T

18:28 interactions, create different effects and we'll that for later. But for

18:33 uh the thing here is that with an infected cell, so you see

18:38 missing, right? Missing these, not present on this cell due to

18:44 infection, right? So it it's or maybe there's only much fewer of

18:52 or, or not at all, ? Due to the result of the

18:55 , right? And that's what the killer cell would see and then go

18:59 . So, so um and even cells can produce these kind of changes

19:06 well. And so you can cancer . So again, it's not a

19:11 , it's not everything but certain virus cells, certain cancer cells do produce

19:17 effect and they can be attacked by killer cell. OK. So,

19:24 so again, these are we call , right? They are your

19:28 identify yourselves as yours, right? , of course, that can go

19:35 that system when you have autoimmune right? Because now you,

19:41 you're recognizing your own tissues as something , right? So there is time

19:46 that, of course, can Ok. Um, any questions about

19:53 C, we'll mention this again as should keep going through, but for

19:58 we're OK. All right. um lymphatic system, so pathetic system

20:07 is think of it as a secondary system. Although there's no hard pumping

20:14 system, it's pretty much gravity and contractions that kind of and,

20:20 and uh contractions of circle bugs because , they're close to each other.

20:26 those movements, um plus muscle grabbing, they kind of help move

20:33 food around. So what is What is this stuff? Well,

20:37 just kind of start here at the . So, arteries and veins through

20:44 . OK. And so of you know, very thin wall,

20:49 narrow, right? That's for exchange material. So all your vital

20:55 right? They, they collect, have the capillary bits in your vital

20:59 how your cells get nutrients and things they waste much, right?

21:05 obviously, fluids coming out, And so it's what we call interstitial

21:10 . OK? And so you of , results in a in a drop

21:16 blood volume. OK. So you of want to get that back,

21:20 . And so as the lymphatic fluid back here on your collarbone, dumps

21:25 into your circle, of course, maintain blood. Ok. So that's

21:31 of one function of lymphatic, very . But the other thing is lymphatic

21:38 . Ok. Vessels can concentrate fairly in certain parts of your body called

21:45 nodes or very dense collections. Right pits, the growing tonsils or lymphatic

21:52 . Uh Yes, there is under skin like that are very thick with

21:56 tissue. In your intestines, you this as well. Um the uh

22:02 in certain organs like your, your will have a intense concentration of

22:06 OK. So the other thing about where these areas are really dense and

22:11 , they're full of B cells and cells and macros and dendritic cell.

22:17 kind of there where they hang OK. And so because of

22:22 for example, in your spleen where have this dense Yeah. Yeah,

22:25 have this and fat tissue, you kind of some help filter the

22:30 right? You can bind to like antigens, bind potential patterns in your

22:37 your your T cells, for that are in there, you can

22:42 shown antigen, they can respond to . OK. So similar in your

22:48 , I think you can just um in uh you can kind of filter

22:54 your saliva and and and these cells affect that way. Uh uh inhaled

23:01 as well. Um So you here's an example of um a couple

23:07 areas of salt and salt sounds kind weird. But these are again dense

23:12 of lymphatic tissue, OK? All types of immune system cells. And

23:17 in your intestines, you have what called these pyres patches, OK?

23:23 purple, these purple blobs are these dense areas of um this lymphatic

23:30 OK. And so here is kind a and part of that structure is

23:36 thing called the M cell that you right here. OK. So here

23:40 your normal um uh intestinal cells that like these micro, right? That

23:48 saw a pen, it's gone So this right here. OK.

23:51 here's an M cell in the So it can trap, trap microbe

23:57 then you have macrophages on the other , for example, that can

24:02 And or show an to your other system cells. And so um the

24:09 here is kind of a like from bat as well where they collect and

24:15 got it also, it's actually also a certain type of pathogens. It's

24:20 way for them to actually survive inside microphage and go further into your

24:25 right? So that's how an intestinal can make its way out for their

24:31 because they had a factor to do . So we'll see some examples of

24:35 later. But uh certain food borne can do this salmonella, they can

24:40 get into your blood supply, then the worst effects. Of course.

24:45 . So the thing to remember, of things kind of put the back

24:47 your head is the intestines in right? Are highly vasal, lots

24:53 capillary, right? Because that's how intestines, that's where you food,

24:57 how it gets to the rest of body and your cell tissues,

25:01 So lots of capillaries in that And so they carry nutrients and things

25:07 rest of your body. But it's a way that pathogens can travel

25:12 right? So again, those for immune system defense, there's could be

25:19 that has a way to bypass it , or use it for its own

25:23 , which I and so similarly, in the skin, you have similar

25:30 of dense areas um under your skin have very dense with fat tissue.

25:37 these B cells, t cells as as well, similar function.

25:43 So, um all the goal of to, if something is in your

25:46 is trying to find it and get of it. Ok. Um So

25:53 , so cytosis. So, so put these little letters kind of

26:01 I don't know, maybe I'll help remember the, the four step process

26:05 . So one is, so your macrophages typically. Um And so the

26:15 is OK, let's let's get them where they're supposed to be this is

26:19 they, there with CS for right? That once they're there,

26:25 should adhere to the pathogen. as a, then take it in

26:32 . Right? I, and then is to digest it. All

26:37 And here ingest digest. Ok. , and so this process, as

26:44 look at um, inflammatory response here a second, there's several side kinds

26:50 are released to attract them to the of infection. OK? Uh Even

26:55 damage, tissues themselves release these chemicals bring them to the site. Um

27:02 adherent. So I remember in this Diran here, here is a close

27:07 of one of those um mps, ? T L Rages can do this

27:13 well. So not only ingest it the bin thing sends off the alarm

27:18 , right? The signal to to more cells involved. Um And so

27:25 . So here is a Lyo and vesical ingestion leads to formation of a

27:33 call it, OK. So they'll and digestive enzymes, radical form,

27:41 kill, kill the uh infectious agent then uh digest um basically just hydrolyze

27:48 , right? Break it down to parts, right? And so some

27:51 those can be recycled. Uh Others expelled. OK? Now, the

27:56 part of this that's, that's not this four letter abbreviation if you will

28:04 Agen presentation. OK? So here be so as it's crunching it

28:11 so to speak like that, you'll formation of MH C molecules occurring that

28:18 bind to these crunched up parts of virus or, or bacteria.

28:27 And we'll bind to it. here's an MH C two,

28:30 And there's a two because it's a , right. Macrophage is dendritic

28:35 And um B cells are your type . You may see type two.

28:41 . So it will show this Now, now that's now other immune

28:49 cells can see this and respond to , right? And um typically it's

28:55 a T cell that will see right? And it has a certain

29:01 , it will do, right? , um so multifaceted, right?

29:08 A uh A can do the T R sensitives out the one body

29:14 right? And digest the the the and then it can show antigen to

29:19 immunes cell. So kind of 33 going on here. OK.

29:25 and this is the nature of this here. It's the nature of what

29:29 what we abbreviate A P see antigen cells. That's what they do.

29:36 show antigen through D molecule. Um OK. So uh let's just

29:47 look at this next. OK. a an additional feature the cytosis is

29:56 but not all things are easily So you have to have a backup

29:59 for that. OK. Um So caption, right? Meningitis spectrum,

30:08 capsule, streptococcus pneumonia thick. So how can you get at

30:15 Because the capsule is kind of covering cell surface, just kind of how

30:21 macrophage, for example, a neutrophil to it and takes it in.

30:24 that's not as easily done when you that capsule. So how can you

30:30 this option? Right. So this basically think of it as an enhanced

30:39 . Ok. You're using chemicals, we call opsonin, OK, to

30:45 with the um taking in the binding taking in the micro. And so

30:53 example, so two things can do antibodies and compliment you can coat the

30:58 or the and then that makes it to take. OK. And so

31:03 that process is optimization. OK. uh so here's an example, this

31:09 be a a by term of the that is easily and here are

31:15 right? That are formed to the . And now the uh and so

31:25 learn probably by the end of the that you know the Y shape um

31:30 a body that we draw um one to the. So let me just

31:35 it like this, these ends by antigen. OK. A G is

31:41 for antigen, right? This OK. A cell combined one of

31:47 cells combined. All right, we'll , we call this the what's called

31:51 F C region. OK. Down . And if you, if a

31:57 has an F C receptor like this does, right? These yellow

32:03 then it combined the antibody at that . So it takes a whole thing

32:08 , right? The whole complex as see here. So here's the F

32:12 receptors, right. Here's the antibody complex. So the whole thing gets

32:18 . We didn't have this, And it was just in this

32:22 it would be much, much lesser being, but having that process,

32:28 whole thing gets taken in. So that uh uh that facilitates basically

32:35 otherwise they wouldn't be easily favor. , you know, and of

32:40 the same thing can happen uh with , we'll talk about that shortly.

32:46 . These are protein factors, the coats the cell and these cells can

32:51 them in. OK. So, let's look at real quick.

33:00 So let me just look at this . So here is the engine presentation

33:06 . OK? So we've got a , for example, uh microbes,

33:15 ? And in the process of that digestion, some of those uh molecules

33:22 to emit c molecules being made goes the surface and the helper cell.

33:29 one of the effects of that again, chemicals released, right?

33:34 cytokine is released as a result. one of the functions is to activate

33:40 macrophage and other macrophages in the OK. So what that means is

33:47 a macrophage does its thing ize it of these, these pseudopods, it

33:55 all right. So the more of forming, right? The that's how

34:02 combined and take things in. So you look at the micrograph over

34:07 all right, you see this guy the corner that's an inactive one,

34:13 ? You see how it's like basically a round ball, right? But

34:17 it gets activated, you see how word is fluffs up, there's one

34:22 , maybe I think about it. these represent lots of membrane folding,

34:27 super pods being formed, right? an active macrophage kind of like got

34:32 flower bloom on the petal right coming . And so more of those means

34:39 of lot more binding taking in making big city cell. So much more

34:46 obviously, that active form is one can really compared to the in active

34:51 . So if they're activated in this by T cell, OK. And

34:59 , that's one effect, there's other that occur. But that's, that's

35:02 big one more presumably this is all because showing an engine it's potentially uh

35:13 may be occurring. Let's get rid it. OK. So um so

35:19 uh how this might look, I something like this here. Um So

35:31 is our bacterium up here, here our the macrophage. So I'm just

35:36 of fast forward to here a little . And so we're gonna get the

35:41 right? The adherence ingestion right here a um So this is the

35:47 of course, when it comes to binding form a lysosome, then and

35:58 we go speed this up a little . So we get digestion and then

36:04 comes MH C molecules being synthesized. Right here. Yeah, here comes

36:16 C molecule and then it will bind with fuse and then bin some of

36:26 nitrogen. OK. Then go to surface and that's how it can interact

36:34 A, no, I like a cell or something. OK. So

36:42 all right, let's look at this here. So we're gonna go into

36:46 response. OK. And uh so gonna be a sequence to this.

36:54 . So we're answering this. So of the things about what do you

36:59 to encapsulate the inflammatory response? A we're talking about the acute ac U

37:07 E acute inflammatory response, which we've gone through at one time or

37:12 Um The purpose is to confine it's regional process. It occurs in a

37:21 part of the body where this infection been introduced. So to keep that

37:28 a local, they'll let it right. That's what the inflammatory response

37:32 about. Keep it contained. And um there's steps that happen,

37:40 course, after that to, to that happen. OK. And of

37:48 involves a lot of different cytokines to different, to do different things.

37:57 . All right. Let's count All right. From 32. That

38:41 . Yeah. So what would this this occurs? Nothing else will

38:46 right. So this has to occur . Right. That's one.

38:54 number two, I'd say it be . Ok. Baso dilation. I'd

39:04 then probably stick above us a wall exit. Then uh, swelling is

39:14 occur and then repair. That'd be guess. Ok, we're gonna go

39:21 steps. Ok. So, so with the acute inflammatory response,

39:34 response, um, keep it contain the effect. Yeah.

39:42 extravasation is the process of because the kills system and that's where you need

39:50 the crime prevention fighters. Um you got to get him out to

39:57 into the area where the offensive And so extra is that process

40:03 OK, to extract, extract them the blood vessels to figure the

40:11 The that the primary one is doing and later on take over.

40:17 So um the example here is sort a basic example but it's just showing

40:28 puncture wound, introducing uh microbes into body, right? So, um

40:38 of course, you're gonna have nearby and wandering around typically. Um the

40:45 and the, and the, and tissues themselves, the damaged tissues here

40:50 can chemicals, right? But certainly in the area can as well.

40:55 so um these have varied functions. what do you, what are,

40:59 are you gonna get other cells to site to help you out? Attracts

41:05 big thing? Ok. Um You then to affect this blood vessel,

41:11 get to manipulate it. Right. get cells out of there, you're

41:15 have to make it more porous. ? Um You've also got to,

41:20 know, your blood flow is going a pretty good speed, right?

41:24 it's not just floating along, I think a cell, it's just

41:28 You know, they're, they're rushing through blood, blood's pumping.

41:33 So, if you're gonna get this out, you gotta slow down blood

41:39 a little bit in, in in the area, in that

41:44 you wanna slow down blood flow and them out, Jack. So,

41:51 so there's gonna be chemicals, that will bring about the different steps

41:55 this process, ok? But first foremost, it's about containing this infection

42:02 there and not letting it spread. basically what the acute inflammatory response is

42:07 . Ok. So how do we down blood flow and actually get more

42:12 to the air, right? More gets more, right? Well,

42:16 manipulate blood vessels. So this is vasoactive factors come in. Ok.

42:22 remember uh dilation of blood vessels, ? They're making them bigger,

42:28 Increasing diameter. OK. So in that, the blood vessels of

42:33 are getting closer to the surface, ? That's, that's what creates the

42:39 in the area of inflammation, Um So making bigger. So now

42:45 slowing down. So we're increasing volume the, in that area. It's

42:49 of the redness blocking and we're also it down, ok? If you

42:57 , um, if you're increasing the of area in the uh diameter of

43:03 vessel in the area, it's going slow it down in that area.

43:07 . So you're getting the two you want lots of blood to the

43:11 and slowing it down, ok? now you can begin to grab onto

43:15 neutrophils and get them out. And so, uh here, this

43:21 here is when they squeeze out like , right? Like this guy right

43:28 , right there. It's happening because kind of in the make up the

43:35 vessel. So these right here lining bug vessel, these are cells,

43:43 ? These are what we call endothelial . And so they're stuck together to

43:48 of loosen them up a little bit allows cells to come in.

43:52 And this, when you see this , that's that thing process called margination

43:59 it kind of squeeze out between the , OK? Um And so as

44:06 result, this area fills up with that help bring about the control of

44:13 infection, basically. OK. So look at some of these steps

44:18 OK. So again, lots of chemicals, right? Uh different

44:24 vasoactive factors, leins, histamine raine you need to memorize all these

44:29 OK? There's a couple that we'll , OK? And so the uh

44:37 , and many of these have multiple functions, OK. So uh

44:43 neos factor is one of those that uh stimulates uh these other subs to

44:51 in and uh Brady Ken helps to of pull apart the connections.

44:57 There are um different molecules that makes stick together. And there's other ones

45:05 you promote. So you can kind grab onto the neutrophils, kind of

45:08 of it as so the neutros can to it and slow down and then

45:15 it. OK? Also this is , right? But these are prostate

45:21 . This is what asper actually the lands bring about pain, right?

45:27 enhance the pain reception in the You you wanna be aware of

45:31 you have something going on here, ? Inflammation wounds and whatnot. But

45:36 know, it makes you aware that have something going on there, but

45:39 can be too much. That's why might take aspirin to kind of it

45:43 shuts down the synthesis of prostate Um uh other things Brady kind of

45:49 . So, degranulation, they work things called mass cells and these have

45:55 you have vesicles inside them and the of makes them get rid of

46:02 And so they release chemicals like ok? Histamine also works on the

46:08 vessel keeps making it more porous, ? Um Dilates it. So um

46:15 you, you kind of keep that going on so you can keep getting

46:20 controls out and keep fighting infection because want want to control infection contain

46:25 Ok. Not let it spread. so, um the um,

46:32 so Turo factor, that's one of that kind of promotes the formation of

46:38 other pros landings. So lots of going on and um the uh these

46:43 are kind of involved in, don't to worry so much about it,

46:47 creator protein has to compliment and so , you may get that involved later

46:52 . But um so let's look at example of this here. Um

47:03 Right. OK. Oops. Now happened? OK. One more

47:22 Oh, goodness. All right. just keep here. All right.

47:26 kind of the same example of kind a splinter wound happening here and let

47:32 shut him up. There we Damn it there. OK. So

47:39 comes our bacteria. You see mast over here, they will can take

47:51 in, they surprise at least set as a result. All right.

47:57 then uh create these other effects. basic act of factors that form.

48:03 so uh close up. And uh , so the blood vessels. So

48:14 is end cells. We're gonna kind first uh produce these molecules that will

48:20 to slow down bind to neutrophils, ? We call them. So

48:26 slow, slow down. Yeah. you'll get some of these other molecules

48:37 but also serves to bind. So kind of slow them down and get

48:41 , more tighter binding going on. these different ICA molecules. Uh but

48:46 all about kind of slowing it down buying it to so it can slow

48:50 and out of the blood system. then uh then we'll loosen up the

48:57 between cells. You very time event and they pop out and then um

49:19 , are something like 70% of of the cells in your blood that

49:23 neutros? OK. And so um , of course, if we just

49:29 how a cell came out, of , other fluid comes out as

49:32 OK. Not just, not just cells. So, you know,

49:36 of been that comes so blood and kind of getting a little bit more

49:44 there. So we have swelling occurring , of course, uh as these

49:47 are fighting infection, uh you're it's gonna, it, it could

49:51 just a mass of dead cells and dead neutrophils that have done their

49:56 And that's what we refer to as so you kind of have that in

50:00 for a while. So, um so scientific information, right? The

50:06 from the div of blood vessels for going to the surface, makes it

50:10 in the area, then uh for and swelling again, a natural process

50:16 you're trying to continue faction out this . OK? Of course, you're

50:20 that in a few days. So um let's see any questions about

50:30 . So, inflammatory response contained the . Now, chronic inflamma inflammation,

50:37 ? So this is something where this kind of gets triggered again and again

50:42 again, that last months and right. So it can be,

50:48 doesn't, doesn't have to be a , you know, it can be

50:52 that you eat, right? Some those things can be antigens that inflame

50:57 , ok? And every time you that particular thing, it can cause

51:02 particularly in your intestines, right? um that's why, you know,

51:07 could be a chronic thing. You these things unknowingly, it'll happen over

51:11 over again, right? So for certain types of things, you

51:14 try to restrict what you eat if the kind of process here. But

51:17 can also be a a chronic infection doesn't really ever go away and then

51:23 kind of triggers periodically over time. can cause that kind of effect,

51:27 example. OK. So uh you , the contrast between these two acute

51:33 is time, right? Chronic um chronic inflammation occurs repeatedly. It

51:39 takes a toll on uh acute inflammatory a few days and you're over

51:45 Ok. So, and you just to complete this. So another

51:49 that can happen at the end So the repair and healing over the

51:56 , that's to be the end of in inflammation process. You're you're healing

52:00 and getting over it. Ok. um so compliment, so compliment if

52:08 look at this in the book, gonna be very complicated. Lots of

52:12 , so that step and that's up that step, OK? I'm only

52:16 really with these right here when this that typically initiate the bulk of the

52:24 of compliment. OK? So number compliment is not a cell,

52:30 Complement are protein factors that are in blood. OK? They're in the

52:36 form, OK? That become activated three different processes. OK? And

52:44 , and so when you see like example, C three, OK?

52:48 or C five. So basically a without a letter after it,

52:53 These are the inactive forms. And the c when it gets activated,

53:00 the active form can then activate the step and then so on and so

53:04 . That's what's like a cascade of like 20 different factors. And

53:09 but again, it's when these C C five get activated where you get

53:14 main effects occur. OK. So way to activate it through antibody,

53:22 something called lectin and through binding to cells, OK. So uh

53:31 antibodies can activate compliment, OK. the effects you see here,

53:36 This is the same no matter how activating, right? So that doesn't

53:41 , it's how you activate that, differentiates these three things, right?

53:45 anybody can activate it um binding to bacterial surface, right? So um

53:54 bacteria, of course, they have types of cell surface molecules very different

53:59 ours. And uh they can uh recognized by compliment and that recognition in

54:05 can activate it. OK. And lastly, is these things called

54:11 OK. Particularly what they call Manno is very common to see on

54:18 surfaces. OK. So, lectin produced in the liver floating out of

54:25 blood and then can bind to bacterial like this and activate component.

54:33 So, however, it's formed. . And so just one point

54:39 So I mentioned a couple of times how adaptive immune system and innate immune

54:45 may, may kind of overlap some and presentation. So too can this

54:52 of activation antibody? Right. antibody is a productive adaptive immune system

54:58 innate. So it's kind of another crossover here. OK. So,

55:03 right. So, however, it activated. What are the effects?

55:07 , the effects are the, so talked about that before, like coating

55:14 pathogen with, with compliment. Uh your cells can have receptors for

55:21 and take the whole thing in Um cytolysis. All right. So

55:26 is the formation of what they call membrane attack complex. OK. So

55:32 different co factors coming together, inserting in the membrane and then causing leakage

55:42 . OK. Because of that um negatives or more successful, right?

55:49 the outer member, right? Membrane positives are less susceptible because they have

55:56 and these and these, these concept form in pepper. They are compatible

56:03 a membrane, not pepper. I . Ok. So ram negatives aren't

56:09 I'm sorry, ram positives aren't as by this. Ok. Uh Then

56:14 can, it can be uh Um pug inflammation, the presence of

56:21 cells combined compliments or remember, mast or types of these different side of

56:26 involved in inflammation. Um the uh cells are also involved in allergic

56:33 hay fever, other types of It's often these guys and they kind

56:39 over. Um but they do have role in, in um in um

56:45 . Ok. So again, all effects can occur no matter how you

56:50 it. Um But again, remember , compliment, not a cell,

56:55 proteins that become activated. OK. Interference. So this is a,

57:04 , there's two types, we talk this in the context of, of

57:10 have against viral. OK. So so two types of interferon. The

57:17 one is the antiviral. OK. And so how it works is by

57:24 virus infected cell will synthesize the OK? And that then becomes

57:36 secreted and others in the area can to it. So, here's the

57:44 . Uh this cell is likely gonna , but the release of interferon can

57:50 all neighboring cells. OK. And the effect is to basically induce gene

57:58 . OK. Being a being an of gene expression, particularly for specifically

58:05 these antiviral proteins. So the noninfected produces these antiviral proteins. Virus tends

58:12 be infected our proteins, basically destroy viral genome. Ok. So basically

58:20 stopping the infection. Ok. Um cells, these cells that are

58:26 Ok. So any, any cell receptors for the interferon contacts it,

58:31 will be protected right through these antiviral . OK. And um it interfering

58:38 . Um This is one of the biotechnology products. It was mass

58:45 thinking it would be a um wonder against all viral infections that turned out

58:50 to be uh but it's, it more an issue of uh bad shelf

58:56 though. You couldn't put it on shelf and, you know, have

58:58 very short duration of it was active . It turned out to be a

59:05 issue. Didn't too much of it was toxic. Ok? But

59:09 is still used, it's used um with severe viral infections, they'll get

59:13 of Interferon as part of the part their treatment. So it is effective

59:18 when it's controlled. Um um but not, it's not something you take

59:22 a pill, you know, form viral infection. Nonetheless, it's still

59:27 in those kind of um as a , your own innate immune defense,

59:31 also as a treatment. Um the two is one that's we talked about

59:38 acidic cell, right? So that's they can do. OK? Um

59:45 them more phagocyte. Uh through this two infer uh increasing MH C

59:51 Ok. So that means they can with more. Uh There's, there's

59:57 be, we'll talk about this but there's T cells that recognize certain

60:00 C A. So if you have of these on you, then you

60:04 can be found out by T cells easily and that will help your immune

60:11 . So, um, the last the innate immune system defenses is

60:17 Ok. So fever, uh although pretty miserable by ha, it

60:25 it is useful for sure. In three ways, it's useful for

60:30 . So, um so this all to the adjusting the body's thermostat.

60:38 , the hypothalamus is your basic, thermostat. OK? And it operates

60:43 a set temperature. Ok. Um temperature much like if you're a bit

60:52 a cold spell, I mean, got too cold and you want to

60:54 home and you want to warm Obviously, you hit the thermostat,

60:59 ? Increase temperature. Ok. um your body responds to pyrogen in

61:06 similar way. Ok. So basically pyrogen are those microbes outside the

61:14 When they get into you, they endogenous pyrogen. OK. And so

61:20 01 is short for uh and so is the actual agent that turns the

61:30 in. OK. So it works the hypothalamus. And so here,

61:33 example, all of us are about C plus or minus half a

61:40 maybe a degree. Ok. Um so preops will increase that,

61:47 So much like you're cold and you to get inside your apartment and crank

61:51 heat up. That's not gonna happen , right? It's still gonna be

61:59 until you, until that apartment temperature warm inside there. Right? So

62:05 , very similarly your body right? you're at that new set point,

62:12 ? You feel cold, it right? So your, your paros

62:17 cracked up. Where's that? But still not there yet, right?

62:23 still feel cold? Ok. um, so what happens?

62:28 as we all know, you get temperature, of course, you're not

62:33 car, right? Because you your body is not meant to be

62:36 at 30 8, 39 40 OK. Of course, you don't

62:41 good. But uh and typically what is you kind of oscillate a little

62:46 , you get the chill, you hot, cold, hot,

62:49 but you're kind of kind of went and forth. Ok. So as

62:52 go up and down, right, slightly elevating that you're slightly lowering it

62:57 little bit, maybe going from 39 maybe 40 to then be 38 a

63:01 or whatever kind of fluctuate. You're time between chills and cold,

63:06 Ok. So what's going on Ok. In terms of your

63:12 well, you are doing these three , right? So a temperature pathogens

63:21 your body like 37 degrees. So you're increasing temperature, slow down the

63:26 . Ok. So remember this thing talked about last time about buying,

63:33 fine. That, that idea, ? Buying time, right? By

63:40 time to do stuff, OK. do it. Pathogens do it.

63:45 ? A pathogen inside a cell is from the immune system. It's buying

63:51 . You slowing pattern and growth through , that's buying you time. So

63:56 immune system can recognize and and your immune system can respond, find

64:01 find the gen, do a right? Buying you time. And

64:05 increasing T cell activity will learn that types of T cells that kind of

64:12 the whole adaptive movement. So activating guys, uh those ones will bring

64:19 activate your whole adaptive immune system. then the other thing here kind of

64:23 to growth again, growth, This does of course, but so

64:27 that we talked about in chapter iron is a baby. In terms

64:33 things trying to grow in your you use it for multiple things,

64:38 love it. I it's all your blood cells, OK? It's how

64:41 find oxygen, but you also use in another way, right? Various

64:46 uh in your respiratory pathway, you ? So you have different uses for

64:51 . Uh So too does the infecting want that stuff? OK. And

64:57 they actually have and so uh lowering causing fever actually lowers the uh you

65:06 put a clamp on the iron And so it makes it very hard

65:11 confidence to get, get at but they actually have chemicals as well

65:16 bind iron. So it's kind of again, uh us versus them and

65:21 to get rid of uh get a of iron. And so in doing

65:25 doing this, of course, will growth as well. So temperature plus

65:30 them of the availability of nutrient. those will help slow the growth

65:34 Ok. So, um anyway, some point, you know, of

65:38 , you, you uh overcome the body but as that gets back to

65:45 and of course you're feeling better. . So, um any question about

65:51 fever or? Yeah. Yeah. , yeah, well, the temperature

66:13 that from is gonna be your habitat I never talk about even you can

66:26 high temperature fuels right now. I it's, it's all you going to

66:33 right. But you have that little that you talking about that could be

66:38 , it's all about, it's all as well. So maybe not really

66:47 football, maybe, maybe, not a lot of sense, but

66:57 into the nineties effectively. You What she did, I hope

67:13 Um let's say you activated cough. , yeah, you, I would

67:21 you can be in the wrong Um But yeah, I um like

67:34 sure is, but you're gonna get All right. So I think we

67:52 a question kind of wrap this up we'll talk. Um I'm only just

68:00 do like a um overview. The slide of chapter 24 basically an

68:08 So I'll just do that one far that. OK. Let me count

68:58 here. All right. 43. . If you answered B you're

69:29 OK. So uh that's either antibody compliment, right? They're not self

69:35 , right? Um It's formed by complement, not mh C molecules,

69:46 , anti antiviral, right? Not a cell. OK. All

69:52 . So don't go anywhere it So here's a summary of the innate

69:59 system defenses. OK? Um So talk a little bit about third line

70:10 . OK. So here, of you're talking about. So you can

70:18 that immune system in the two OK. Hum Vus. Some,

70:23 think of those as extracellular pathogens, pathogens. OK. So uh B

70:32 types, humor, immunity antibody OK. So we have B cells

70:40 type uh that uh develop into. the whole vaccination thing is about forming

70:52 but also forming memory cells. So don't produce antibodies, but they,

70:57 basically a record of what they've responded before hand. So we see it

71:03 , then these cells forming antibodies. . So you do both of these

71:11 it's first time exposure, whether it's vaccination or dispute infection. Um And

71:18 course, you find antibodies can't get of a cell and deal with the

71:22 that they're gonna deal with that virus it's outside the cell. So it's

71:26 pathogens. Ok? Now your um cells and let me just say

71:33 when you start reading this in chapter it goes way more than and not

71:39 give you the whole story here because know, you, I'm only talking

71:44 most of the times you'll, that part of the process, but there's

71:48 . OK? Um You can we offer immunology course if you really

71:52 get into all of it. Uh I'm trying to just keep it,

71:56 know, just keep kind of Let's go on. OK? But

71:59 just another, there's more to it you get the basics, OK?

72:06 that deal with like a different but a natural killer cell deals with infected

72:12 . OK? That result is to get rid of the killer, basically

72:16 the affected cell but it's still You call those to key cells,

72:24 ? And then other T cells like we call T helper cells,

72:30 And that's differentiating and some of these work with um um OK. B

72:41 which is a type of an presenting , but they have their own specific

72:44 helper cell type. OK? Um macrophages and dendritic cells work with T

72:51 type ones and then you see differentiation the class type Mh C two.

72:58 C one. So to T cells the body cells, right? Liver

73:03 , skin cells, brain cells, tissue type cells that are affected,

73:10 ? That's what these guys do. so uh so it's division of,

73:14 labor, what's going on here with extra patterns in patterns and then activating

73:21 cells of your immune system. So, uh so that's why T

73:27 are really, we have their hands a lot of different aspects of the

73:33 . OK. Very important. And , uh, and, and,

73:37 , HIV, right, uh uh a specific type of these T helper

73:45 and cell really devastates the immune system a result. So, um,

73:51 right, that's it, folks. we'll pick it up

-
+