Okay, so this is Gil Pratt here. This is the second part on cytokine storm, and I laid kind of the

base of the pyramid and probably some of the most important stuff in the first lecture. But

let's get in a little bit deeper into a cytokine storm, but let's step back for a second and

maybe talk about something that we see very, very frequently in tons of inflammatory states,

which is an elevated C-reactive protein.

If you ask your colleagues or maybe yourself, what is a CRP, a lot of people just say it's an inflammatory marker.

The ones that are little smarter might say something like it's an acute

phase reactant and a sign of inflammation, which is basically an inflammatory marker. And then

the really smart ones might tell you that CRP is synthesized in the hepatocytes, meaning in the liver,

and others will tell you that you will see an elevated CRP in response to elevated IL-6, interleukin 6, which is produced by macrophages,

amongst other things. And in return, CRP binds to phospholene on microorganisms, and as a result,

it sets off all kinds of things, which also enhances phagocytosis by macrophages.

And the point being is that the immune response is very complicated as That has just one parts of literally hundreds of the

immune response, but one that's frequently tested in patients with disease processes like

SARS-CoV-2, as well as a lot of inflammatory processes when we're trying to see, one, if there's a ton of

inflammation there, and sometimes trying to see if it's

getting better or worse. And so you have all these cytokines involved in the so-called

cytokine storm. So you got interferon and interleukin and TNF, tumor necrosis factor. Let's just take

tumor necrosis factor, which increases vascular permeability, or let's take interleukin 6.

There's tons of different interleukins. What does that do? Well, it increases antibody production.

Yet, as I said, it also increases CRP.

So it's not that you don't want interleukin 66 made, it's not that you don't want CRP made.

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