Innate Immunity Lecture

Question 1

Innate Immunity

Answer 1

the routine protection that we have at birth; it’s what we’re born with in our bodies (skin, phagocytes, lysozyme in saliva)

the reason why we have it is because our body is a nutrient-rich place for microbes to grow

Question 2

Adaptive Immunity

Answer 2

develops throughout life as body is exposed to microbes or foreign material

think antigens and antibodies

Question 3

Antigen

Answer 3

they stimulate the production of antibodies that bind and target them for destruction; they are the the biomolecules on the bacterial cell surface that are detected by antibodies

think adaptive immunity: think T-cells (help make antibodies to fight bacteria when you get sick), B-cells

Question 4

Antibodies

Answer 4

what your body makes to find and destroy antigens

Question 5

Primary response vs. Secondary response

Answer 5

Primary Response: they are the first responders that deal with the bacteria once it’s detected –> B-cells
primary response is supposed to differentiate cells and recognize them as bad and LEARN to make the correct antibodies

Secondary Response: this is based on your immune system’s memory, so if you’ve seen the antigen before, your body will recognize it and be able to make boat loads of the correct antibody to fight against it –> T-cells

Question 6

B-cells

Answer 6

They are WBCs that make a specific antibody to stick into the antigen on the bacteria, which then sucks them in so that they get eaten up. Once they get eaten up they are broken down within the cell –> they have MHC-II complexes that stick out to relay info about the bacteria to T-cells

(this is part of primary response)

Question 7

T-cells

Answer 7

T-cells are helpers cells that bind onto MHC-II and antigens and create cytokines, which go into the B-cell

Question 8

Cytokines

Answer 8

creates by the T-helper cells once they’ve bound onto the MHC-II complex, and they create:

1) Memory B-cells: remembers and can make antibodies when it recognizes past antigens w/o the help of T-cell

2) Plasma cell: creates boatloads of correct antibodies

Memory B-cells and plasma cells are part of secondary response, once you body has seen this antigen before

Question 9

First-line defenses for the body: SKIN

Answer 9

-difficult for microbes to penetrate, think the dermis (tightly woven fibrous connective tissue) and epidermis (many layers of epithelial cells, the outermost part is dead which repels water to maintain a dry environment)

-cilia on the mucous membrane make mucous so that when the bacteria gets stuck on it, the cilia is able to move the mucous away from the body

-only issue with skin is obvious stuff like bites, and wounds, ways to get into the body

-Staph is Gram (+) which means that it’s thick peptidoglycan walls stop it from drying out really easily, which is why it often lives on the skin

Question 10

Mucous Membranes (General)

Answer 10

they exist in digestive, respiratory, and genitourinary tracts, and they are constantly being bathed in secretions (w/the skin it’s literally mucous)

Peristalsis of intestines (automatic movement of intestines), mucociliary escalator of respiratory tract remove microbes (cilia wafts stuff out of you)

Question 11

First-line defenses: Antimicrobial Substances

Answer 11

-Salt accumulates on skin from perspiration
-Lysozyme degrades peptidoglycan (in saliva and tears)
-Lactoferrin and Transferrin bind to iron (so that bacteria don’t use it and duplicate bc they use it as a nutrient)
-Defensins form pores in microbial membranes (form of AMP = antimicrobial peptide)

Question 12

Lactobacilli

Answer 12

all up in the vaginal canal, and it makes lactic acid which lowers the vaginal pH, making it more acidic —> GOOD thing because that way it’s fighting against bacteria!

Question 13

First-line of defenses: Norma Microbial Flora

Answer 13

They are good for you because they:
-are competitive, which excludes many pathogens (they take up space/nutrients so other bacteria can’t use it)
-produce toxic compounds (E. Coli in intestinal tract to make colicins which keep bacteria away)
-disrupt normal microbiota which can predispose someone to infections (candida albicans in vagina create yeast)
-are essential to the development of the immune system (think M-cells)

Question 14

Primary Pathogen

Answer 14

if you’re perfectly healthy, this will still make you sick no matter what; think of the Black Death

Question 15

Opportunistic Pathogen

Answer 15

only causes a disease if it’s somewhere it isn’t supposed to be

for ex) PTD: pelvic inflammatory disease
happens when there is bacteria that goes up your vaginal canal into somewhere in your body (like in between your fallopian tubes) and then you get sick

Question 16

Antibiotic Prescription

Answer 16

the reason why you’re supposed to finish your prescription of antibiotics is so that you’ll actually kill all of the bacteria; the issue is that if you don’t then the bacteria now have something to use to learn and grow resistance to that particular antibiotic

Question 17

M-cells

Answer 17

they kinda live between cells with cillia in the lumen (gut) and basically what they do is chew up bacteria that arer passing by, and that way your body can use it to make antibodies against it

that process is called “priming” and that happens in the immune system BEFORE Adaptive Immunity kicks in

Question 18

Cell Communication

Answer 18

inflammation requires communications between immune cells based on their antigens and it allows for a coordinated response; there are 3 things used:

1) Surface receptors “eyes” and “ears” of the cell
2) Cytokines are “voices” of the cell
3) Adhesion Molecules

Question 19

Surface Receptors

Answer 19

Form of cell communication, serves as the “eyes” and “ears” of the cell; they usually span the membrane, and connect the outside to the inside

-they bind to specific ligands to induce a response
-binds to antigen to tell you that there’s something you need to be worried about

Question 20

Cytokines

Answer 20

form of cell communication, the “voices” of the cells; they are produced by the cells themselves and they bind to appropriate receptors to induce changes: growth, differentiation, movement, cell death

they respond to a surface cell binding to an antigen cytokines which cause inflammation and fever

act locally, low concentration, and you don’t want it to go everywhere or else you’ll go into shock

Question 21

Adhesion Molecules

Answer 21

form of cell communication, it allows cells to adhere to other cells

think molecules on WBCs that interact w/epithelia that lines blood vessels

Question 22

Microbe-Associated Molecular Patters (MAMPs and PAMPs)

Answer 22

MAMPs are detected by Pattern Recognition Receptors (PPRs- think TLRs and NLRs) and they’re basically just anything that’s on the outside of a bacterial cell that antigens from our body recognize as “nonself”

what happens is the body see/attaches/reacts to it, and that’s when your body responds with inflammation

Question 23

Toll-like Receptors (TLRs)

Answer 23

they are anchored in the membranes of a WBC, and they monitor the extracellular environment, and each TLRs has a receptor that detects different things (like one might be specific to look for LPS and bind to something like the O-Antigens)

they just see and detect essentially

once the TLR binds to the bacteria, the binding initiates a change within the cell which induces cytokines and leads to inflammation

Question 24

NOD-like receptors (NLRs)

Answer 24

they are rooted in the cytoplasm of a WBC and they detect microbial components or cell damage

they’re in the cell and once you have degraded bacterial cells, the receptors detect nucleic acids –> looks at what’s inside bacterial cells (DNA + RNA)

Question 25

Complement Fixation System

Answer 25

A bunch of proteins in blood/lymph and they are part of innate system (not adaptive, you always have it)

general f(x) is to kill bacteria through:
1) enhancing phagocytosis by “optimization”
2) directly lyse bacteria (they form holes in the bacteria’s membrane)

Question 26

Optimization

Answer 26

C3b binds to bacterial cells and foreign particles, promotes engulfment by phagocytes that attach to opsonins (like C3b)

optimization is part of the compliment fixation system, it adds antibodies to bacteria so it’s easier to recognize it and get ingested —> leads to phagocytosis being faster (so in like 20 minutes instead of 2 hours)

Question 27

Opsonins

Answer 27

part of the complement system; whatever will make phagocytosis more efficient

Question 28

Inflammatory Response

Answer 28

C5a attracts phagocytes to area; C3a and C5a increase permeability of blood vessels; induce mast cells to release cytokines

components open up blood vessels so WBCs can get to the tissue which ends up with BP lowering (C5a + C3a)

Question 29

Lysis of Foreign Cells

Answer 29

Membrane attack complexes (MACs) are formed by proteins C5b, C6, C7, and C8, and C9 molecules assembling in cell membranes of Gram (NEG)

Question 30

3 Ways the Complement System Starts

Answer 30

1) Classical: antibody binds to bacterium
2) Lectin: protein that binds to a specific sugar on the bacterium
3) Alternative: binds to LPS layer (you make C3 convertase which cleaves/splits C3)

Question 31

C3

Answer 31

an enzyme called C3 convertase that splits C3 into C3a and C3b

C3a: opens blood vessels up so that WBCs can leave to go find the bacteria in the tissue (the process of WBCs leaving the blood vessel into is called Extravasation)

C3b: opsonin; surrounds bacterium and envelops it, and
it can combine w/other proteins to create C5 convertase.
Also, when the body is not being invaded all the time, it aids in making C3 convertase as well

Question 32

C5

Answer 32

C5 is broken down into C5a and C5b by C5 convertase

C5a: acts as a chemoattractant and surrounds the bacteria to tell the WBCs where to go and attack

C5b: lodges itself into the membrane of the bacteria and makes holes while also attracting with other proteins (C5-C9) with its binding site to also make holes in the membrane

They lock into the membrane right next to each other, so they end up making a hole in the bacteria, which disrupts their membrane and they explode

Question 33

Inflammation stuff

Answer 33

edema is when blood floods to one infected area so the tissue gets swollen with fluids; the hope is that WBCs kill bacteria and don’t bring it back to blood vessels and cause sepsis

Question 34

Regulation of Complement System

Answer 34

Regulatory proteins that bind to C3b to inactivate it, since it’s what makes C3 convertase when the body is being invaded (C3 can split on it’s own naturally, but C3b makes C3 convertase which speeds up the entire process

Question 35

Phagolysozome

Answer 35

phagosome w/lysosome attached to it where the lysosome dumps toxic acidic stuff into it to destroy it