00:00
So, M1 macrophages.
00:03
They have a greater capacity
to kill.
00:05
They have more lysosomes.
00:07
They have a
greater oxidative burst.
00:09
They make more reactive
oxygen species.
00:11
They make more nitric oxide.
00:13
So as they say, they are
lean, mean fighting machine.
00:16
And they also make a lot of other
pro-inflammatory mediators
coming from arachidonic acid.
00:22
So those are the eicosanoids
and the other mediators.
00:24
That's the M1 population.
00:26
The M2 population
is going to be important
for regulating, healing,
and scar formation.
00:31
They are going to make
coagulation factors.
00:33
They're going to make
angiogenic factors.
00:35
And they're going to make
collagenases and protease inhibitors
that will allow a scar to form.
00:43
Together,
the M1 and M2 populations
orchestrate the local cell
proliferation activation
by elaborating
a number of cytokines.
00:52
So in this <inaudible>,
in this kind of collection
of inflammatory cells
that get recruited
after the acute phase,
there's a lot going on.
01:01
And it's kind of a sequence
between the M1s killing,
cleaning things up in the M2s
healing, and turning things off.
01:11
Alright, so let's accumulate
the macrophages into the tissue.
01:14
We've talked about
how we're going to activate them.
01:15
Let's get them in there.
01:16
And the macrophages
and the monocytes
are wandering through
the bloodstream.
01:20
And they are recruited
through adhesion molecules,
the selectins and the integrins,
like we've talked about,
with the chemotactic mediators.
01:29
And the chemotactic mediators
are mostly going to be
CXC chemokines,
but can be other things elaborated
by bacteria, or pathogens.
01:37
As we've talked about.
01:39
They get recruited into
the extravascular space.
01:42
They actually have the capacity
to divide.
01:45
So whereas, neutrophils
crawl out and die in 10 hours,
and they don't do anything else
other than die,
Macrophages have the potential
to divide.
01:55
So that we can get
more, and more, and more of them.
01:58
They're also going to be
elaborating mediators
that will call in more macrophages.
02:01
So it can be a pretty aggressive
recurrent process.
02:07
We also are going to elaborate
in that area.
02:10
We want the macrophages
to stick around.
02:13
So we will secrete cytokines
that say, "Hey, stay put."
So we will get recruitment.
02:20
They will divide
in their local area,
and we'll corral them.
They'll stay put.
02:25
So we're going to keep them
in one area.
02:27
And when we get a collection
of macrophages,
we can actually see those
as a distinct entity.
02:33
A little focus of these
activated macrophages
sitting in the tissues.
02:38
When we see it
as a collection like that,
we recognize it as a granuloma.
And it's in a red box here,
because this is an important term
that you need to know
for your pathology
and for kind of generally
understanding processes.
02:52
So granuloma,
just a definition,
is an aggregate,
a nodule of activated macrophages.
03:00
Straightforward.
03:01
Nodule of activated macrophages,
granuloma.