in this video we're going to talk more details about ex A. Toxins and how they can cause damage to the host and so damaged by exa toxins is actually highly specific and these eggs a toxins can actually be grouped based on the type of tissue that they cause damage to. And so for example neurotoxins are going to be exa toxins that damage the tissues of the nervous system. And because they cause damage to the nervous system, these neurotoxins can potentially cause paralysis. Now entero toxins are exotic toxins that cause damage to tissues of the intestinal tracked. And so because they cause damage to the intestinal tract, they can cause things such as diarrhea and or vomiting And then last but not least the cida toxins are eggs, a toxins that damage different cell types by interfering with the cellular mechanisms or by causing sell license And so for example side a toxic T cells which are actually part of our immune system produce cida toxins that kill infected host cells. But of course there are some pathogens that can produce sido toxins as well. And so if we take a look at our image down below notice the left hand side over here is uh an image focused on neurotoxins which again are extra toxins that are going to be damaging the nervous system. And so notice here we have this pathogen, these blue microbes here that are producing these neurotoxins that damage the nervous system and could potentially cause paralysis. The middle image over here is an image focused on entero toxins which again are toxins that are going to be causing damage to the intestinal track. And so notice here we have these microbes and blue once again and they are going to be producing these entero toxins which are in yellow, those little yellow circles and again they can cause potentially diarrhea and or vomiting and then last but not least over here on the far right we're showing you an image of Sido toxins And so of course our side a toxic T cells are capable of releasing Sido toxins these little purple circles that you see here in order to induce uh sell license of infected host cells. And so again some pathogens are also able to use or release Sido toxins as well. Now also recall from some of our previous lesson videos that um exa toxins can also be categorized based off of their different structures and functions. And so moving forward in our course, we're going to be talking about these categorizations which include a B toxins, membrane damaging toxins and or super antigens. And so these are three different types or categories of exa toxins that we'll talk about moving forward. And so this here concludes our brief lesson on exotic toxins and how they can cause damage to the host and we'll get to learn more as we move forward. So I'll see you all in our next video

in this video, we're going to discuss our first major group of exa toxins which are the A. B. Toxins. And so the A. B. Toxins. Once again our exa toxins and they actually consist of two parts, as their name implies, with A. And B. And so the two parts of the A. B. Toxin are the A subunit and the B subunit. Now the A. And a subunit stands for the A. And active. And so the A subunit is also known as the active sub unit. And it turns out that this a sub unit is usually going to be an enzyme and it is going to be responsible for all of the toxic damaging activity of the A. B. Toxin. So of this entire A. B. Toxin, it's really the A. Or active sub unit that is going to be responsible for the toxic damaging activity. Now the B sub unit is going to also be known as the binding subunit. And so the B. Stands for the B. And binding and the B. Or binding subunit is not necessarily toxic. And the B. Or binding subunit as its name implies, it's going to dictate the very specific type of cell that the A. B. Toxin will bind to. And so the B. Subunit or the binding subunit is gonna dictate the binding of the A. B. Toxin. And because once again the B. Or binding subunit is not necessarily toxic, it's the A subunit that is toxic. What this means is that the B subunit can be isolated and separated from the A subunit and then the B subunit can be recombined with medicines so that those medicines can be delivered to very specific cell types. And so this is an area that is being researched and explored even today. Now the A. B toxins can actually infect host cells and a three step process that's being shown down below in this image. And so if we take a look at this image down below, notice over here on the far left hand side, we're showing you the A. B toxin right here at this location. And once again, the A B toxin has two sub units. It has the A subunit or the active sub unit which is the portion that's responsible for the toxic damaging activity. And then it has the B sub unit or the binding subunit which is not necessarily toxic but is important for binding to the specific cell types, binding to specific receptors on specific host cells. And so what you can see here is in the first step, the B subunit binds specifically to a receptor in the host cell surface. And that's exactly what we see Over here, the B subunit is binding to the cell receptor on the host cell. Now in the second step of a Bt toxin um process both the A. And the B sub units are going to enter the cell via endo silicosis. And so here in this image you can see that both the a and the B sub units of the 80 toxin are going to be internalized into the host cell. And recall that when endo psychosis occurs that uh these uh A. B. Toxins are going to be brought into the cell and an end acidic vesicles. And so that's exactly what we see over here on the right hand side is the end acidic vesicles that results from endo psychosis. And so what you'll notice is that both the A. And the B. Sub units are inside of this end acidic vesicles. However, the A subunit, which is again the active sub unit is able to leave the end acidic vesicles and enter into the cytoplasm of the cell. And in the cytoplasm of the cell, the A sub unit is going to be active and it can target cellular functions and inhibit cellular functions such as inhibiting translation here, translation is being blocked and this M. RNA cannot be translated into the protein and that is because of the catalytic activity of this. A sub unit of the A. B. Toxin. And so blocking translation could potentially be toxic and cause damage to that cell. And so this year concludes our brief lesson on A. B toxins and we'll be able to get some practice applying these concepts as we move forward. So I'll see you all in our next video

in this video we're going to begin our lesson on the second major group of exa toxins which are the membrane damaging toxins. And so again the membrane damaging toxins are exa toxins. And as their name implies, these are toxins that are going to damage or disrupt cytoplasmic membranes. And by damaging or disrupting the cytoplasmic membranes, they can cause license of the host cells. Now really there are two main types of membrane damaging toxins. There are the pore forming toxins or the P. F. T. S. And then there are the phosphor a light paces. Now the pore forming toxins or P. F. T. S as their name implies, are gonna be toxins that create pores or in other words, holes in the fossil lipid bi layer of the host cell. Therefore causing sell license Now the phosphor light paces are going to be specific enzymes that are going to cleave or breakdown or hydra lies phosphor a lipids in the cytoplasmic membrane again causing sell license. And so if we take a look at this image down below, we can get a better understanding of these membrane damaging toxins. Notice on the left hand side we're showing you the pore forming toxins or P. E. F. T. S. And which will notice is that here we're showing you the pft and it can bind to very specific cell receptors on the host cell and that can lead to an accumulation of P. F. T. S. And this accumulation of P. F. T. S. Can ultimately end up generating a poor and the poor is once again basically just a hole and the whole can cause cell license and lead to death of the host cell. Now, over here, on the right hand side, what we're showing you are or is an image of foss fogo light paces and again phosphor light paces are enzymes that are going to break down or cleave fossil lipids. And so the fossil white cases are being represented as little tiny molecular scissors here and which will notice is that here we have a fossil lipid bi layer and notice that these fossil white paces are actually able to cleave and break down components of the fossil lipid violator through hydraulic sis, breaking them down. And that is going to disrupt the membrane and once again cause sell license and kill the host cell. And so this year concludes our brief lesson on the membrane damaging toxins. And once again we'll be able to get practice applying these concepts as we move forward. So I'll see you all in our next video

in this video we're going to begin discussing our third major group of exa toxins which are the super antigens. And so the super antigens are exa toxins that inappropriately stimulate helper T cells ultimately leading to the overproduction of cytokines. And so recall that cytokines are a group of chemicals that are used for communication purposes and can help stimulate and generate immune responses. Now these super antigens, the way that they work is that they bind to major historic compatibility complex two molecules or MHC two molecules on antigen presenting cells or a Pcs. And by doing that they cause helper T cells to recognize and respond to antigens that they normally would not be responding to. And so it causes helper T cells to respond to harmless and potentially self antigens which is not good. And so by doing this it can lead to excessive proliferation and activation of the helper T cells and it can also lead to a massive release of these cytokines. And when there's a massive release of cytokines this is referred to as a cytokine storm. And so a cytokine storm is really just a massive release of cytokines. And so cytokine storms can actually be life threatening and they can cause fevers inflammation and even shock. And so if we take a look at our image down below we can get a better understanding of these super antigens. And so what you'll notice is the image on the left hand side is showing you um the immune response and the absence of super antigens. And then the image on the right hand side is showing you the immune response in the presence of super antigens. And so let's start on the left hand side, the absence of super antigens. And so in the absence of super antigens, the T cells which have T. Cell receptors or T. C. R. S. Will only bind to and recognize antigens that are presented on MHC Class twos on antigen presenting cells. And again the T cells will only generate a response to the correct antigen or antigens that are dangerous and harmful and therefore it warrants an immune response. And so without super antigens you get a normal immune response. Now in the presence of super antigens which are again a group of eggs, a toxins the super antigens will bind to the MHC class two molecule. And in doing so when even when the incorrect antigen is presented such as perhaps a harmless self antigen uh it will cause the helper T. Cell to recognize this incorrect antigen and generate a response to this incorrect antigen when it's not supposed to that's what the super antigen does. It causes the helper T cells to generate an inappropriate response and that inappropriate response will lead to the release of cytokines. And over time this will cause a cytokine storm a massive release of cytokines which again can be life threatening. And so this year concludes our brief lesson on super antigens. And we'll be able to get some practice applying these concepts as we move forward. So I'll see you all in our next video.