So this is one of our videos about bacterial pathogenesis, specifically looking at how bacteria might attach or adhere and invade. So when we talk about attachment, it means basically the ability of the bacteria to stick to the cells in your body. And so attachment can also be adherence, and when we talk about attachment, we talk about adhesions.
And these would be things like pilli or Fimbriae. We talked about those in the context of bacterial structure. So if you remember bacteria might be coated in these kind of like hair like projections on the surface and those might be pili or fimbriae. They might remind you a little bit of a flagella, but the flagella is usually longer and that's for motility whereas the pili and the fimbriae are either involved in in this case attachment or if you remember the pili also can be the sex pili for conjugation. And so these are kind of hair-like features on the surface of the bacteria that allow them to attach.
When we think about invasion, we can either think about active or passive invasion. So passive invasion would really be bacteria that are allowed to get into your body through some sort of wound or cut. So they're not necessarily actively doing anything. They're passively being allowed to invade that body.
So then active invasion. means that the bacteria is doing something to get in. And so when they do that, they're usually using something called invasins, which is kind of a general term, just like adhesins, to get in. So I have two really cool key examples to talk about with both attachment and invasion. Okay, so the first example I'm going to talk about is an attachment example.
And for this example, we're going to talk about EPEC, or enteropathogenic E. coli. There's some indication that ehec or enterohemorrhagic E.
coli, like E. coli 0157H7, also does this specialized form of attachment. And this is a really unique form of attachment, but it's kind of a nice way to illustrate what can happen.
So E. coli are gut bacteria, and some forms of E. coli can cause foodborne illness. So what they do is they have to actually have a way to attach to your gut intestinal epithelium. So if you remember, your gut intestinal epithelium...
is a single cell layer of columnar epithelial cells. So all these are your columnar epithelial cells' single cell layer. And so when E. coli comes in, in order to attach, it's basically a three-step process. So the first step is to have some sort of initial engagement with those intestinal epithelial cells using these guys.
And these are BFP. bundle forming pili. So you have this kind of initial engagement and interaction between the bacteria and the gut intestinal epithelial cells. That leads to the second thing, step, which is just a generalized attachment.
And so at this point they're somewhat attached but they're not necessarily stuck. And when you think about your gut and you think about how much stuff is moving through your gut, we really need a stronger form of attachment in some cases in order to really mediate a disease like state. So the way they do this is they do this third step that's an intimate attachment. Intimate. And so this is what's really the cool part here.
So what they do is, going back to my bacterial cell here, they use what's known as a type 3 secretion system. So I'm going to call this type 3 secretion system, or TTSS. And the type 3 secretion system, if we were to zoom in on this, On the surface of the bacteria, it's built in the cell membrane through the cell, through the outer membrane of the E.
coli as well. And it looks like a giant syringe. And it literally is a whole bunch of proteins that are built to look and operate like a syringe.
And what that does is that, so this is happening in the, you know, surface of our bacteria up here. So this is our bacteria. The bacteria then can make proteins that they deliver through that syringe and if this syringe is right up against an epithelial cell then those proteins will get delivered into that epithelial cell so if we go back over here those proteins are getting delivered into these gastrointestinal epithelial cells so what actually happens I'm going to give us a clean screen here for just a second so let's zoom in a little bit let's look at our gastrointestinal epithelial cells And we have our E. coli kind of sitting on the surface here. And we had the bundle-forming pilli that had that initial interaction.
And then we have this type 3 secretion system, which is like basically a syringe. And so that syringe is going to inject proteins into this host cell. One of the proteins it injects is something called TIER.
And so TIER is actually a host cell receptor. And so it will get tracked. up to the host cell and it'll end up in the membrane.
Okay, so if this was happening in multiple cells, right, I'm not showing it this way, but let's say these tier host cell receptors will actually be expressed by the host cell. What's cool about tier is that it is not normally found in our cells. It's something that is strictly bacterial.
And so, but the bacteria, this has a way to actually make sure that this protein is expressed on the membrane of your gut cells. And then Tyr binds to Intamin, which is actually already expressed on the surface of the bacterial cell. So this one's called Intamin.
And so these two will interact with one another, and they kind of mediate this tight attachment. So first thing is that... When we talk about pathogens, we usually talk about them having to have specific receptors to interact with or bind to host cell receptors. So you can actually have that pathogen to host interaction.
But in the case of EPEC, it injects its own receptor into your cells and then uses that to bind to a receptor on its surface, Intamin. And so now we have this receptor-receptor interaction, but it's all bacterial mediated. And they can only do this because they use that molecular syringe, that type 3 secretion system.
Okay, so this is a really cool portion of attachment, but what's actually also happening is that with this type 3 secretion system, we're injecting a whole bunch of other stuff. I'm going to switch colors for just a second here. So we're going to inject other things into the host cell.
And what those other things do is they interact with the cytoskeleton. So if you remember, you have the cytoskeleton in your cells that help kind of provide the structure. And so what happens is these host cells go from being like this, kind of this nice tight single cell layer with bacteria attached on top.
And remember, they're attached through intamin to tear. And we have this attachment happening here. But these host cells, because they've now also injected these proteins that mess up the actin cytoskeleton, all of a sudden this host cell will be modified so that it kind of makes this weird-looking pedestal.
And that pedestal, with this intimate tear interaction, provides a really, strong intimate binding between the bacteria and the host cell. And so we call this pedestal formation by enteropathogenic E. coli. So that's pretty cool. So the next example we're going to talk about is actually an invasion example.
So for EPEC, they really are totally content with just attaching and having this nice intimate form of attachment on the surface of your cell, so they don't necessarily have to get in. But for Salmonella, they want to invade your cells because then they're going to move into your cells and then move into other aspects of your body. They become a little more systemic more often than not. And so Salmonella in your gut also interacts with your gut epithelial cells, that first line of defense, that single cell layer. And so they have an initial interaction through invasions, just like anything else.
And then they get close enough and then they also use a type 3 secretion system. Okay, so type 3 secretion system. And they're going to inject proteins into the cells just like the other one.
But instead of injecting a cell surface receptor like E. coli does, they actually inject just things to really mess with that actin cytoskeleton. And so they're going to kind of interfere with a whole bunch of... cytoskeletal effects in this host cell and the end result of that is really that the host cell is going to start to do this ruffling effect. And so now instead of making a pedestal they make these kind of weird ruffles and this might be happening on a single cell basis or maybe a couple cells are being affected at the same time but what ends up happening is that we make this kind of weird ruffled thing out of the normal cell shape and then the bacteria eventually engulfed.
So they're going to be engulfed by this epithelial cell here and then brought in so now they're actually inside the host cell and then from there Salmonella knows how to like get in and do its thing both inside the cell and eventually beyond that initial cell layer. This is referred to as membrane ruffling and it's a very specific process also mediated by that initial interaction of invasions. and then another type 3 secretion system.
There are really good animations of both of these types of examples, these events, also included with your videos to watch for this module.