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.
The lecture Accumulating Macrophages in the Tissue by Richard Mitchell, MD, PhD is from the course Acute and Chronic Inflammation.
A granuloma is...?
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