發炎反應 (英)

Back

⇐ Use this menu to view and help create subtitles for this video in many different languages. You'll probably want to hide YouTube's captions if using these subtitles.

發炎反應 (英) : 發炎反應的概述

相關課程

0 / 750

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 dlated.
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 margination.
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.