Name: How Inflammation Really Works | Institute of Human Anatomy
Uploaded: 2024-11-18T18:13:26.000Z
Duration: 17 min 48 s
Description: Thousands of YouTube videos with English-Chinese subtitles! Now you can learn to understand native speakers, expand your vocabulary, and improve your pronunciation...

Inflammation is quite the misunderstood process.

It's frequently thought of as a bad thing, and that we need to do everything we can in order to get rid of it.

But inflammation is actually about healing.

And so when inflammation is working properly, this is a good thing and it's absolutely necessary.

Because without this incredible process, we would not survive.

Now, it is true that there are situations where inflammation can become chronic with specific inflammatory conditions and certain lifestyle choices.

But today, let's first talk about how inflammation is supposed to work by discussing some of the amazing signals that your body utilizes when it's injured or under attack.

And how these signals change your blood vessels, change your white blood cells, and promote this incredible natural healing process that we call inflammation.

Inflammation Now, all of us have experienced inflammation in some form.

Maybe it was from an injury like an ankle sprain, a splinter in your finger, or some sort of pathogen like bacteria that's trying to invade you.

But regardless of the cause, there are some common signs of inflammation which include redness, swelling, heat, pain, and sometimes loss of function.

Like with an ankle sprain, you've likely experienced all of those signs, including the temporary loss of function with that joint.

Or maybe you've had a pathogen infect your tonsils, and they got red, hot, swollen, and painful.

And what we're going to find is that all of these signs of inflammation have a purpose.

Or in other words, can be explained by the steps of inflammation that we're going to cover now.

So let's use this picture to help us with this.

So, as you can see, we have a tiny little blood vessel here called a capillary.

And inside the capillary, you have this cell representing a white blood cell called a neutrophil, which is doing this really cool roly-poly process that we'll get into during the next step, and we'll find that it's not really called the roly-poly process.

But outside the capillary, we have some tissue cells that I've taken the liberty of drawing in myself.

And as you can see, they are sad and injured.

Now, as I mentioned earlier, this all starts with some sort of tissue and cellular injury.

And this injury could come from trauma, where connective tissues and cells are damaged and torn apart, or from a pathogen like bacteria that could release harmful toxins.

And we are representing these scenarios here with this star-looking inflammatory explosion.

But this injured tissue will release multiple substances.

And we have some of those substances labeled here as these blue cytokines.

And these cytokines will initiate the inflammatory response by signaling to nearby troops as well as distant troops that it's time to go to war.

And these troops are your white blood cells.

The first white blood cell that gets called into action is a tissue macrophage, which I've drawn here as this large blob cell with a purple nucleus that actually kind of looks like a mouth, but that kind of works because this cell is going to engulf things.

But this response to these damaged cells occurs within minutes because a tissue macrophage is a local macrophage that resides in the actual tissue in this area.

And this is really cool because essentially, you can think of it as your body stationing troops, these tissue macrophages, in the tissues throughout the body, just in case something like this happens, so that you can have an immediate response, again, within minutes.

And these tissue macrophages participate in a process called phagocytosis, which translates to cellular eating.

They can engulf dead tissue, cellular particles, as well as pathogens such as bacteria.

And this step takes place during about the first hour of inflammation.

Now, this first step with these tissue macrophages is very important and even life-saving.

But the number of these tissue macrophages is not very high.

And so there isn't enough of these troops, especially in more moderate to severe injuries and infections.

But luckily, those chemicals or those cytokines that were released at the start of inflammation also signal to more distant troops for additional backup.

And after about the first hour of inflammation, large number of neutrophils, another type of phagocytic white blood cell, will start to infiltrate the inflamed area from the blood.

This infiltration was caused by those inflammatory cytokines.

And for you physiology nerds out there, maybe you've heard of some of these cytokines like tumor necrosis factor and interleukin-1.

But these names are not necessary to have an understanding of this process.

But these cytokines and other biochemical products produced by the inflamed tissues initiate some really cool processes that allow for this infiltration of the neutrophils to occur.

First, as I've already hinted to, the cytokines attract the neutrophils to this actual site of injury.

Kind of like putting up the bat signal or radioing for backup.

And using these chemicals to attract the white blood cells to this site of injury is referred to as chemotaxis.

Second, these cytokines also cause increased expression of adhesion molecules on the surface of the endothelial cells that are near the site of inflammation.

Now, endothelial cells are just the cells that line the capillary.

But if you look at this picture, we can see that these adhesion molecules on the endothelial cells, one of which is called selectin, and the selectin will interact with the integrin molecules on the surface of the neutrophil.

And this essentially will cause the neutrophil to get stuck or adhere to the capillary wall so that it doesn't get pushed past the site of inflammation with the blood flow.

What is also happening at the same time is that the cytokines and other inflammatory signaling molecules cause the capillary to vasodilate, which is to increase the diameter.

And this brings more blood and therefore more neutrophils to the site, as well as causes the intracellular attachments between the endothelial cells of the capillary to loosen, creating larger gaps between the cells.

And this increases the permeability of the capillary, which will cause more fluid to leak out of the capillary and into the site of inflammation.

But it also allows our roly-poly process to occur where this neutrophil army can kind of army crawl across the capillary wall and then squeeze through the cracks between the endothelial cells.

These neutrophils are now at the damaged tissue site where they can help those tissue macrophages defend and clean up the area through phagocytosis.

Now again, it isn't technically called the roly-poly process.

And the names are, again, not really as important as the concepts.

But for those of you that love names, when the neutrophil adheres to the endothelial cells, this is called marginination because it attaches to the margin of the capillary.

And when the neutrophil squeezes through the cracks between the endothelial cells, it's called diapoditisis.

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Now, let's have a little bit of a checkpoint here.

One, if you had to pinpoint one of the most important take-home messages about inflammation, it is this process that we just saw.

Getting these white blood cells to this site of injury or infection so that they can clean house and initiate the healing process.

And we are also starting to see why we experience some of the symptoms of inflammation such as red, warm, and swollen.

Remember, I said that the capillaries vasodilate and the spaces or the cracks between those endothelial cells get wider.

And this led to not only the neutrophils getting out of the bloodstream to the site of injury or infection, but also allowed for fluid, some of the plasma from the blood, to leak out of the capillary and into those tissues.

And this is what accounts for the swelling and the increased warmth and redness.

The swelling can also lead to some pain and discomfort as the tissues and nerve endings start to get compressed and stimulated.

There's also an interesting distinction between inflammation caused by trauma or injury versus inflammation caused by some sort of pathogen such as bacteria or viruses.

With both scenarios, you get the process that we've described so far.

But with an injury, say like an ankle sprain, you also add some additional damage.

And what I mean by that is with something like an ankle sprain, you're literally tearing through tissues such as ligaments.

And the severity of this tearing can obviously vary based on the severity of the sprain.

But you will also potentially tear through capillaries that supply that tissue where whole blood literally spills out of those torn capillaries.

And this will typically contribute to even more swelling as well as the addition of bruising because now you have red blood cells and other components of the blood spilling out of the torn capillaries that don't typically spill out of the intact vasodilated capillaries that you would see with, say, something just caused by a pathogen or I should say inflammation just caused by a pathogen.

And obviously, tearing through soft tissues with injuries is also going to come with some additional pain.

But again, in either scenario, bringing the white blood cells to the site of injury or infection is one of the most important parts of this story.

So much so that we actually even have a second wave of white blood cell troops sent to the tissue.

Within a few days of inflammation starting, a white blood cell known as a monocyte will come from the blood and enter into the inflamed tissue.

Now, you might be thinking this monocyte is a completely new cell.