Placeholder Image

Subtitles section Play video

  • >>Dr. Ketchum: So we are going to go ahead and continue our discussion of the immune

  • system, and well be discussing innate immunity. Now before we discuss innate immunity, you

  • need to understand that there’s actually two different types of immunityone of those

  • being innate immunity, which is also called nonspecific immunity, and the other is called

  • acquired or adaptive immunity, which is also known as specific immunity. But just to give

  • you a quick overview of both of these, when you first think about the nonspecific or the

  • innate immunity, it’s a very rapid response. This is your first line of defense. And what

  • this does is it gives your body time for the specific immunity to kick in. So innate immunity

  • is always there. It’s present; it’s going to happen as soon as your body is invaded

  • by a foreign object, and then the specific immunity will take over after that. It’s

  • rapid, and it’s also not selective. So it’s not targeting specific species of invaders,

  • for example. It’s not specific. It just wants to kill foreign invaders, and that’s

  • the end of it. The innate immunity involves physical and chemical barriers, and it also

  • includes cellular defenses. Now once the innate immunity has occurred, then the next type

  • of immunity that will occur or kick in is the acquired immunity. It’s a slow response.

  • And so because it’s a slow response, it’s very selective in what it’s killing. It

  • may kill a specific bacterial cell or a specific virus, and specific immunity includes two

  • different types of responseshumoral responses, which are also called antibody-mediated responses,

  • and cell-mediated responses, which are also called cytotoxic lymphocytes. Here’s our

  • analogy. When you think about an innate response, the castle is the body. And the first thing

  • that this innate response wants to do is it wants to prevent that invader from entering

  • the body. And once that invader invades the body, then the innate response will have some

  • other methods for killing the invaders as well. These things are all taking place as

  • the acquired response is just getting startedbut remember it’s slow, so it takes a while

  • to get the acquired response going.

  • So neutrophils, the eosinophils, basophils and monocytes are all cells that are important

  • in an innate response. The lymphocytes, on the other hand, are the type of white blood

  • cell that are important in the acquired response. You don’t have to memorize the amount of

  • each of these cells in a microliter or their diameters or any of that. You need to understand

  • their anatomical features and their functions. So these are important columns here, but you

  • do also have to know their abundancetheir relative abundance. So again, if you remember

  • Never Let Monkeys Eat Bananas,” that tells you the most abundant leukocyte all

  • the way to the least abundant leukocyte, which are yourbananasor your basophils,

  • so that way you don’t have to memorize the amount per microliter. The reason this is

  • important is because if youre looking at a slidelet’s say you take a blood smear

  • on a microscope slideand, and this is a healthy person, and youre going through

  • and youre identifying all the various white blood cells. Well if youre finding more

  • basophils than you are neutrophils, then youre probably not correctly identifying those cells.

  • Okay, so here’s a flow chart that I put together to help organize the innate versus

  • the adaptive response. So youre definitely going to want to use this as your road map.

  • Were discussing the innate responses in this part, in part two.

  • First let’s start with the physical and the chemical barriers; you think about these

  • as being the wall of the castle. So the first thing I’d like to discuss are the lysozymes.

  • So you have lysozymes that are in your tears and other secretions. These are not lysosomes;

  • lysosomes are different. Lysozymes are antibacterial. So when you cry, it’s actually a good thing

  • because youre killing any kind of bacteria that’s on your skin. You also have the skin,

  • then, and the skin is a physical barrier. The skin also has fatty acids and normal flora

  • as well thatll affect the pH and some foreign invaders cannot survive on the skin just because

  • of the normal flora on our skin. Then you have the mucus and the cilia that line the

  • trachea. The mucus traps any formed particles, and then the cilia works that debris up the

  • respiratory tract and into your mouth so that you can either swallow it or spit it out.

  • If you swallow it, it goes down into your stomach. And remember, the stomach has a pH

  • of two; it’s very acidic. So it’s likely to kill most invaders, but not all. Now taking

  • a closer look at the skin, were not going to spend time on the skin. This isn’t anatomy,

  • but you should realize in this course that you do have two major skin layers: the epidermis

  • and the dermis. So pay attention to those two layers and know where those two layers

  • are locatedwhich one’s on the outermost which ones on the innermost.

  • The dermis, then, the only thing that you need to know about the dermis are the sebaceous

  • glands, and I want you to use your textbook to figure out what’s the function of those

  • sebaceous glands? Why are they important in the immune response? Then we have inflammation.

  • So inflammation is part of the innate immunity as well. When you think about inflammation,

  • it’s your body’s response to tissue damage or microbial invasion. So youve sprained

  • your ankle and your ankle is now inflamed. You stepped on a nail, andso now you have

  • tissue damage and microbial invasion by stepping on a nail. So the goals of inflammation are

  • listed here for you. You want to bring phagocytes to the injured area, because if you can control

  • those invaders at the area that theyve invaded, then they can’t spread throughout

  • the body. You want to stop them there. So if you can bring those phagocytes to the

  • injured area, you can destroy, inactivate invaders, you can remove any kind of cellular

  • debris, and you can start preparing for healing. So let’s take a look at this flow chart.

  • The leukocyte that automatically will start phagocytizing as soon as invaders enter into

  • that wound are your macrophages. So those macrophages are there, and they immediately

  • start attacking foreign invaders that enter the wound. The bacterial invasion itself and

  • the tissue damage as well can cause the mast cells to release histamine. Histamine then,

  • we know, causes vasodialation. So when an arterial vasodialates that means you have

  • less resistance, right, and therefore more blood flow to the injured area. So because

  • there’s more blood flow to the injured areathat’s why it becomes red and that’s why it gets

  • hot. So because there’s more blood there, that means that you have an increase in certain

  • plasma proteins that may be important in the healing process. So these may be clotting

  • factors, for example, that would prevent you from bleeding out.

  • The release of histamine by the mast cells also increases the capillary permeability.

  • So what I want you to do is think about a capillary here, and I’m just going to draw

  • three endothelial cells that are forming the walls of this capillary. And when you have

  • histamine release, the pore size has increased significantly. So if you increase the pore

  • size, that means more fluid can flow through those pores. So that means youre going

  • to get a local accumulation of fluid, some of that fluid being in the interstitial fluid.

  • Remember that weve talked about swelling or what we call edema, an excess of interstitial

  • fluid. It can also cause pain, because you have excess fluid in an area and the skin

  • can only stretch so muchthat causes pain. Pain is a good thing, because pain actually

  • forces you to rest whatever part of your body is injured, and that way it can repair itself

  • if it’s resting. Because you have this increased capillary permeability, then that’s going

  • to increase the number of phagocytes that can make it to the tissue, like your macrophages.

  • If you have more phagocytes, that’s going to increase their secretions. And their secretions

  • can cause systematic responses like fever, for example. All in all, then, this is an

  • inflammatory response and all of the information in red herethese are all cardinal signs

  • of inflammation. And all of these cardinal signs of inflammation are because you had

  • changes in blood vessel functionthe blood vessel vasodialated.

  • When we talk about phagocytosisthis is a form of endocytosis, but specifically, how

  • is it achieved? So it’s going to be your job to fill in the steps. Don’t go into

  • moreany more detail than what these four steps are asking for here. Opsonins, I do

  • want you to look at opsonins and, and, why do we need opsonins? Why are opsonins important

  • in phagocytosis? Then we have interferon. This is another type of innate immunity, and

  • the goal of interferon is to interfere with viral replication. Now many of you have had

  • Intro Zoology and so you know that when a virus gets inside of a cell, the virus takes

  • over the machinery of that cell. And so it starts producing it’s own viral RNA and

  • it’s own proteins. So there are some other functions of interferon that are listed here,

  • and go ahead and read them and at this point realize that there are other functions for

  • interferon besides interfering with viral replication. So let’s take a look at how

  • this will work.

  • Were going to take a cell, and it’s been invaded by a virus. So what the cell

  • doesonce the cell is invaded by the virusthe

  • cell is going to be releasing interferon. So the interferon is going to enter the extracellular

  • fluid, and it’s going to travel to healthy cells, cells that have not been invaded by

  • the virus. And when it binds to these receptors on an un-invaded cell, this un-invaded cell

  • now will produce inactive enzymes. So basically this cell is just waiting, it’s waiting

  • to be invaded by a virus. Because what these enzymes will do once they become activated

  • is they will break down viral messenger RNA and theyll inhibit protein synthesis. Now

  • here comes our virus; it invades this cell. So those inactive enzymes are now active enzymes.

  • Were going to stop protein synthesis of the virus. So if a virus cannot multiply inside

  • of a cell, the virus is dead. Viruses rely on cells in order to make their own proteins,

  • and they, again, take over the machinery of the cell. So if they can’t do that they

  • have nothing to survive on. This is why we call it interferon. Interferon is interfering

  • with a virus; it’s interfering with its replication. So next we have the natural killer

  • cells.

  • Natural killer cells are kind of like lymphocytes. Theyre important in the innate response,

  • and theyre going to release some chemicals called perforins that well discuss here

  • in a second. Theyre going to target cancer cells and they target virally infected cells,

  • and theyre going to lyse the membranes of those cells. So let’s look at how natural

  • killer cells work. This killer cell here is a natural; so it binds to the target cell.

  • Once they come into contact, the natural killer cell releases perforins. What perforins do

  • is they create a pore in the membrane of the invader. So if we do that then water and ions

  • can rush in. We increase the permeability. So if you increase the permeability for water

  • and ions into the cell, the cell will swell and burst. It’s going to lyse. Then we have

  • the compliment system. The compliment system is activated by two different means. The only

  • one well discuss here is listed here at number one. We will discuss number two here

  • later, but first, let’s focus on number one when we activate a compliment system.

  • So here you have a bacterial cell, and on the surface of it is some carbohydrate. That

  • carbohydrate is recognized by a compliment protein. So these compliment proteins are

  • floating around in your plasma. That’s where theyre located; theyre in the plasma

  • cruising around. And when the compliment protein recognizes this carbohydrate chain, the compliment

  • protein will bind to the plasma membrane of this bacterial cell. And once it binds to

  • the plasma membrane that creates a whole cascade of events that end up developing what’s

  • called a membrane attack complex, a MAC. So this membrane attack complex is essentially

  • a pore. So once you develop the pore, fluid can rush into the cell, and then the cell

  • will burst and it will lyse. So that kills that target cell as well. So compliments really

  • good in killing bacterial invaders.

  • So innate responses are really good. Theyre quick, but they have their limitations. Theyre

  • not specific; theyre not going to kill specific bacterial species, for example. And

  • theyre also short-termthey don’t last very long. So the problem with it is that

  • because theyre short term and theyre not specific, then you have to have a smart

  • system, and that’s what adaptive immunity is all about. So in the next part were

  • going to start discussing adaptive immunity, and specifically, were going to look at

  • characteristics of your B and your T cells.

>>Dr. Ketchum: So we are going to go ahead and continue our discussion of the immune

Subtitles and vocabulary

Operation of videos Adjust the video here to display the subtitles

B2 immunity innate response invaded fluid specific

Human Physiology - Innate Immune System

  • 1418 46
    SylviaQQ posted on 2015/09/12
Video vocabulary