Inflammatory response | Human anatomy and physiology | Health & Medicine | Khan Academy

By Adem Lewis / in , , /

We’ve all had cuts on our finger
or wherever else on our body, and immediately that part
of the body gets a little bit of redness, a little bit of
swelling, some heat maybe, and, of course, there’ll be
some pain associated with what’s going on there. And in general, this set of
symptoms that we experience, these are known as the
inflammatory response, or you might say that there’s some
inflammation going on there. And people have known about this
I guess ever since really people have been having cuts. I think probably with modern
medicine, people have been a little bit more particular about
actually classifying the symptoms, but this isn’t
anything new for someone to say that there’s some type of
inflammation going on or some type of inflammatory response. But what I want to do in this
video is understand what’s causing these– I guess we can
call them macrosymptoms. What’s happening at
a cellular level? Because, really, the
inflammatory response is essentially the initial
field of battle of our immune system. Our first line of defense is our
skin or the fluids on the outside of our skin or the
mucous membranes, but the inflammatory response is what
happens when something gets beyond that. We get punctured with a nail, or
there’s some type of virus or bacteria gets beyond our
skin or the mucus that surrounds our membranes. This is the field of battle,
especially the initial field of battle. So let’s set up an immune battle
so we can see exactly what’s going on with the
inflammatory response. And I want to be very clear. Immunology, is still a very
under understood field. It’s an area of active
research. People are still discovering
the mechanisms and it’s hugely complex. I’m sure we’ll probably
be studying this for a long time to come. So what I’m going to talk about
is just the overview, just you know the general actors
and you know in general what’s causing the redness,
the swelling, the heat, and the pain. So let me draw some
skin cells. This is a gross
oversimplification of everything, but it’s really just
to give an idea of what is going on. So I’m going to do
a cross-section. So those are some skin cells in
there, and then I’m going to– so this is the outside
world right here. Then amongst those skin cells,
I’ll do some other cells. We’ll talk about what they do. I won’t go into huge
detail about them. Let’s call this cell right
here a mast cell. I’ll draw a few more
mast cells. Maybe another one right there. That’s a mast cell. And if you remember from the
videos on phagocytic action or phagocytes, you’ll remember
there was one type called dendritic cells and they tend
to hang out near our skin. They kind of hang out near areas
that might interface with the outside world. I’ll draw a couple of dendritic
cells and these are also the ones that were
really good at activating helper T-cells. They’re called dendritic
cells. They have no relation to
the nervous system. They just look like they have
dendrites on them and that’s why they call them dendritic,
but they’re really phagocytes and they tend to be near
external interfaces and they phagocytose particles and
they’re good at presenting them to helper T-cells so that
they can get activated and ring the alarm bell,
so to speak. So this is just a normal,
functioning, happy skin. So that’s the outside. Over here, this is the
interstitial fluid. That’s just a fancy word for the
fluid that cells are kind of being surrounded by
or that bathe cells. The cells aren’t all directly
connected to the circulatory system. The oxygen goes from the
circulatory system to the interstitial fluid and
eventually finds its way into cells. So everything is directly
connected to capillaries, but capillaries play a big role
in our circulatory system. So let me draw that. Instead of just drawing them as
tubes, I’m actually going to draw the cells of our
circulatory system. So let’s say that this down
here– these are the endothelial cells of
our capillaries. So these are literally the cells
that make up the walls of our capillaries. And of course, this is
a cross-section. If I were to– I would draw
it as a tube somehow. It’s not like it’s a sandwich. It’s actually a tube. Everything is in
cross-section. So these are capillary
endothelial cells, and of course, right in here, we have
our blood flowing and we’ll have red blood cells in here. These are red blood cells. Maybe they’re flowing
in that direction. On this side, they’re
oxygenated. This would be arteries and then
they’d become veins as the red blood cells
lose their oxygen. And of course, you might have
circulating white blood cells inside of your– obviously, in
much lower quantity than your red blood cells, but just to
show that they’re circulating and they’re moving with your
circulatory system being pumped by the heart. Now under normal circumstances,
there is an exchange obviously of gases
between what’s going on in our circulatory system and the
interstitial fluid and there’s also a mild exchange of some
cells and proteins. What we’re going to see
now is what happens when we have an intruder. So let’s say someone takes a
nail, dips it in some cow manure, and then pokes
you with that nail. Let’s see what happens. So let’s say someone pokes
you with this nail dipped in cow manure. So it’s got all sorts of nasty
stuff on it, pathogens on it, probably has a bunch
of bacteria sitting in the cow manure. I didn’t pick cow manure
at random. It’s probably a good
source of bacteria. So as soon as it pierces the
first line of defense, as soon as it pierces your skin,
a couple of things are going to happen. A lot of these bacteria are
immediately going to start floating around in your
interstitial fluid. The cells that it came in
contact with, it pierced them. It probably killed some cells. It’s also going to damage some
of these skin cells and those skin cells are immediately
going to start releasing chemicals, the ones that are
still in a position to do so. They’re going to start releasing
chemicals that are essentially chemical messengers
that move through the– well, at first locally in
the interstitial fluid and says, something is going on. Something has happened to me. And these are called
chemokines. And chemokines are just a very
general word, really, for small molecules or small
proteins that cells release as a kind of signaling mechanism. Chemo for chemical, kine for
kinetic, for moving. These are messengers. They move. So these chemokines
get released. And this is all tremendously
complicated. So I’m doing very high level. There are many, many types
of chemokines. And also you have these mast
cells here, and these mast cells can be activated by direct
contact maybe with the rusty nail. It could be from the chemokines
released by some of these cells up here. It could be from some of the
molecules released by the actual bacteria. These bacteria are also
releasing different byproducts as they enter the body. And any of the above can
activate the mast cells and mast cells release histamine. So you can already appreciate,
I’m doing a high-level overview, and it already is
kind of complicated, but I think you get the sense
of what’s going on. And if the word histamine sounds
vaguely familiar, it’s probably because you’ve taken
an antihistamine sometime probably in the last
several months, especially during cold season. Histamine is kind of one of
the main actors in the inflammatory response, and when
you have a cold and a runny nose and stuffy nose and
all of those type of things, those are all byproducts of the
inflammatory response, and anti-histamines essentially
try to shut down that inflammatory response so some
of those symptoms disappear. But it begs the question
of is that necessarily always a good thing? Because, as I’m going to talk
about in this video, this is the first line of defense. This is the first part of the
battle of our immune system. But anyway, so the histamine–
one of the things that the histamine does is it goes to
the endothelial cells that line your capillaries, and it
causes them to separate away from each other and make the
actual capillaries larger. This is called vasodilation. Let’s say that they’ve all been
activated with a little bit of histamine. The histamine has come
in so now these guys get further apart. They get further apart
and the actual capillary becomes larger. So this is where you get a lot
of your swelling, because all of sudden, the capillary’s
larger, more fluid, and actually, it gets smaller
further down so it really encourages the fluid to collect
right around here. So this is called vasodilation,
just another fancy word for saying your capillaries are getting dilated. They’re getting larger. Fluid is filling them up. Not only are things starting
to collect here– more and more red blood cells are
collecting here, obviously there’s a lot of fluid here,
the white blood cells– but also the capillary walls are
becoming more porous. All of a sudden, things that
couldn’t get through them are going to have a much easier
time getting through them. And one of those things that
are going to have an easier time getting through them– and
once again, remember, all this other stuff is going on. You have these histamines that
are being dumped on these endothelial cells and
maybe some of it ‘s getting into the serum. You have these chemokines being
released locally from this area of damage. You have the actual things
being– the green was the color of the molecules being
released by the viruses. You have the chemokines,
which are in blue. They’re all being
released here. And so the first responders,
the phagocytes, and in particular, the neutrophils,
which are the most abundant of the phagocytes, a subclass of
white blood cells, they’re attracted to these chemicals. They want to move in the
direction that there’s more of these chemicals. And now that the space between
these capillary cells have gotten further apart, they
can get through. So what they actually do is–
let’s say that this right here is a neutrophil. They start kind of rolling along
the wall right here. That’s called marginalization. They roll along this wall and
eventually– so they kind of stick to the wall. They adhere to the wall, and
then eventually they squeeze through these gaps in
the capillary wall. This is called diapedesis
or extravasation. Sometimes it’s called
emigration. These are all fancy words,
but essentially it’s just squeezing through the walls. So that’s the neutrophil
right there. And then, of course, because of
the vasodilation, this is where the neutrophils will be
getting dumped in and this is exactly where they’re needed. So these neutrophils are going
to be here and then they’re going to do what they do. They’re going to phagocytose
some of these bacteria and start eating up, and
maybe even some damaged cells up here. And so that’s what you
want to happen. That’s why I said this is
the field of battle. At the same time, your dendritic
cells, other phagocytes, they will eat up the
viruses and then they’ll present them on their
surfaces. And it’s not just neutrophils
that are coming in. Because this is kind of an area
of congestion and all of the fluid is coming here, you’ll
also have B-cells and T-cells that’ll also
make their way. They’ll also experience
marginalization, where they roll up against the sides of
the capillary and then diapedesis or extravasation
where they go through, and then they’ll be activated, and
they can actually do the specific immune system. So the whole point here is I
wanted to show you– and this is why I delayed the whole
video on the inflammatory response, because it isn’t just
one type of simple thing. It’s actually the field of
battle where all of the actors come and play, even the first
line of defense of your skin, and then all of the actors, the
nonspecific reactions of– inflammatory response is
normally categorized as nonspecific because it’s going
to happen no matter what comes, but you have the
nonspecific actors like the neutrophils. You have your specific actors
like your B-cells and T-cells and you also have the
nonspecific complement system. And I’m not going to go into
detail here, but you actually have proteins that are flowing
in your blood plasma that are normally in an inactive state,
but when the inflammatory response occurs, these proteins,
they get essentially activated and sometimes– and
this is all not 100% well understood– they become
activated, they get cleaved up, and then the cleaved-up
versions of those proteins are really good at, in a very
nonspecific way, helping to kill off at least some of what’s
getting– maybe the bacteria in this case. So this right here, this is the
complement system, which is really just a set of proteins
that always just floats around and they are a
good kind of first line of nonspecific fight against some
type of invading pathogen. So hopefully, this gives you a
good sense of what is going on in the inflammatory response. And as you can imagine, you have
all of this fluid coming here, all of this blood
is collecting here. You have all of this fluid
coming into– so not just cells that are going from
our capillaries into our interstitial fluid, you’ll
actually have fluid going in and that fluid that’s going
in is called exudate. So this whole thing become
swelling and red and engorged and that’s why you see, on kind
of a very macro level, these type of symptoms. Anyway, hopefully, you
found that useful.

100 thoughts on “Inflammatory response | Human anatomy and physiology | Health & Medicine | Khan Academy

  1. have a degree in applied bio science and now getting a degree in bio-molecular science thanks to Khan academy! hahaha

  2. khan! Wbcs initially flow medial and rbcs rather lateral. This is due to their size. Upon inflammation this changes. Rbcs start binding to each other, in result influencing viscosity, and low bp. When these rbcs are binding with each other they actually become larger than wbcs in size, which just means, much the same like the latter, though the reciprocal now. Rbcs start to flow medial as the wbcs move lateral, marginalize and start to bind to the endothelial cells via selectins, intergrins, ciliated sugar molecules, i, v and p cans, etc, etc. Mast cells, which are just basophils in the tissue release histamine and influence vasodilation. Endothelial cells will shrink and you will start to see what it appears to look like nodes. Through these nodes will wbcs and protein molecules will pass through. The latter is responsible for the swelling in respect to inflammation and the former for the pigmentation and temp.

  3. the most amazing video ever you should get paid for university lectures coz u make students life hell easier keep up the harwork:)

  4. oh my goodness i think once i graduate im going to have to credit it to you and your videos 😀 this is where i learn.. not really at my lecture

  5. I could not have better words to explain how awesome your idea of teaching worldwide. You deserve huge respect…….

  6. i'm a bit confused, not a bit though, anyone know the whole cells that contribute in inflammatory response? just mention it, you don't have to explain the function if you don't want to. thank you.

  7. I've seen dozens of videos about inflamation, and none of them makes me understand it the way you do!

  8. Just a tip for people who are watching these videos: It is still very easy to understand at 1.25 or 1.5 speed. This way, you can get through this vdeos faster but you still learn just as much.

  9. Does this apply to broken, torn, or otherwise damaged muscles? or to sprained, broken, or otherwise broken bones?

  10. Thank you! I've had trouble understanding how the inflammatory response works and even after a 3 hour lecture I still didn't understand WHY you got swollen etc. This really cleared it up for me and I understand it a lot better. Thank you 😀

  11. Wow this was so helpful. Thanks a lot. I like your drawings/sketches, letters, the accent and mainly your cool attitude.

  12. 12:06….. Our white cells are like the U.S. MARINES coming to the rescue!!!! 🙂 They're first on the scene…..

  13. Did you say arteries become veins? I don’t think that’s true but maybe I’m taking your words too literally.

    Thx for the videos btw!

  14. I've been struggling the entire semester, just to hold a low C in Microbiology. My daughter told me to check out Khan Academy because it has been her saving grace throughout Nursing School. I want to thank you Khan Academy. Just from the few videos that I've watched so far, I know I still have a fighting chance to pass this class! You are an Angel, sent from Heaven and truly appreciate what you do! I'll come back here to update with my final grade in May. I just couldn't wait that long to thank you for these videos! I don't even know how to explain how wonderful of a teacher that you are! I love you!

  15. I think you forgot the 5th parameter of inflammatory response; "functiolesis" or loss of function – if inflammation affects a mobile area of the body such as a joint.

  16. whenever i have exam i come to this site to understand more and teaches me a lot. and i always get a high marks on every test.

  17. Why don't you create the visuals beforehand? You're needing to draw often forces you to slow down the presentation at points and it really messes with the flow. In addition you could create better visuals since you're not attempting to render them in real time. I suppose one could make the argument that the real time drawing engages the viewer but I don't buy it.

  18. If you wanted to know, the IgE-primed mast cell releases granules and powerful chemical mediators, such as histamine, cytokines, granulocyte macrophage colony-stimulating factor (GM-CSF), leukotrienes, heparin, and many proteases.

  19. So obviously this is how the body deals with an invasion but why would you want to stop this response? I always hear blah blah blah about inflammation an how it's to be avoided at all cost. In short I'm having a crisis if context

  20. Out the utmost respect for the Romans and Ancient GreekZ, and the Hyperfanzification of the video, the Four Typical Signs (And Symptoms or The Clinical Evidence or Expose) of Inflammation are really Hyperemia, Edema, Pyrexia and Hyperalgesia to mean what was said to be Redness (Rubor), Swelling (Tumor), Heat (Calor) and Pain (Dolor).

  21. Amazing. I have behcet and always wanted to learn more about inflammatory reactions. In my case there isn't an external factor triggering it,or maybe there is but it is minimal and doesn't justify the inflammation. Does anyone know where I can find more information about how Bechet inflammation occurs? I know it involves TNF cells,but not much more

  22. This video is so helpful I’m going to cry! Thank you from a very stressed out nursing student days away from a pathophysiology exam 🙏🏼

  23. What does cyclooxygenase do then? I understand that NSAIDS inhibit and that cyclooxygenase forms prostaglandins & thromboxanes

  24. At 50yrs old decide to get my GED and go to my community college. Kahn academy was my tutor I got my GED in December started my community college classes the following January.

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