Lecture 10 Innate Immunity Flashcards by Sara Fieger

immunity present before any exposure from pathogen

effective from time of birth

immunity

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first line of defense is composed of

innate immunity

skin

mucosal membranes and their secretion

normal flora

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second line of defense

innate immunity

phagocytosis (NK cells) (neutrophils, eosinophils, DCs, macrophages)

inflammation

fever

antimicrobial substances

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what is the third line of defense?

Adaptive immunity

specialized t cells and b cells
Abs

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chemical barriers of innate immunity

defenses
lysozyme
complement

active in opsonization

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qualities of skin that make it a strong microbial barrier

it is a tough physical barrier (hard to get in)

dry, salty environment, acidic (hard to survive)

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Lysozyme

works by cleaving Nag/Nam (bond connecting sugars) in peptidoglycan

effective against gram + cells

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ciliary escalator

mucous secretions trap microbes and pushes them away from lungs

either towards throat (for digestive system) or into mouth to be coughed out

goal is to keep them out of respiratory system

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where is lysozyme found?

tears
secretions
mucous

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what keeps the lower respiratory system sterile

ciliary escalator
alveolar macrophages – phagocytes of lungs

prevent microbes from growing here

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what parts of the body are sterile

lungs

bladder (kidney to bladder)

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what can be found in the stomach that prevent infection

gastric acid

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what can be found in the intestines that prevent infection

pancreatic enzymes
bile
intestinal enzymes 
GALT 
peristalsis \shedding of epithelium
secretory IgA 
normal microbiota 
paneth cells

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Paneth cells produce

produce lysozyme

produce cryptins

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what do they eyes have to prevent infection

mucus secreting membrane

Tears: lysozyme, lactoferrin, secretory IgA

lacrimal apparatus that flushes microbes

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sebum

forms protective acidic film over skin surface to inhibit microbes

first line of defense

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saliva

lysosome, urea, uric acid to inhibit microbes

IgA to prevent microbe attachment to membranes

slightly acidic to discourage microbial growth

first line of defense

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gastric juices

destroys bacteria and toxins in stomach

first line of defense

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vaginal secretions

slightly acidic to discourage bacterial and fungal growth

first line of defense

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inflammation

confines and destroys microbes

imitates tissue repairs

second line of defense

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NK cells

kill infected target cells by releasing granules of perforin and granzymes

they then kill infected microbes

antimicrobial substances of second line of defense

complement
interferons
iron binding proteins

effects of complement activation

opsonization (phagocytosis)
membrane attack complex (cytolysis)
attract phagocytes

How do NK cells know which molecules to target?

Fc receptors– bind to Fc cells on Ags

where do all three complement pathways converge?

C3 Convertase

C3a, C5a result

mediate inflammation (stimulate histamine release) phagocyte recruitment

C3b result

opsonization of pathogens (enhances phagocytosis) removal of immune complexes

C5b, C6, C7, C8, C9

form MAC leakage of cytosol --> lysis

what is released by complement that stimulates inflammation

histamine

how do bacteria evade complement

capsules (prevent C activation so no complement) inhibition of MAC formation enzymes that target C5a (no inflammation so no phagocytosis)

complement protein deficiency would be worse for which protein?

C3 all complement would activity cease

IFN- a and IFN -B

geared for viruses cause cells to produce antiviral proteins that inhibit viral REPLICATION don't neutralize virus itself

IFN-Y

geared for bacteria causes neutrophils and macrophages to phagocytize bacteria

how do IFN- a and IFN -B work?

they don't alter the virus itself, instead they inhibit viral replication of neighboring cells so virus can't spread

where do TLRs bind?`

PAMPs

what do IFN- a and IFN -B secrete to prevent attack on neighboring cells?

antiviral proteins (AVPs) these cells prevent attack viral transcription in neighboring cells

what are structures unique to microbes that we use to group them?

PAMPS

example of PAMPS

peptidoglycan LPS flagellin

what recognize PAMPs on phagocytic cells?

PRRs esp. TLRs

what type of PRRs function exclusively as signaling receptor?

TLRs

what is the ultimate outcome of PAMP-TLR activation

signals inflammation

mechanism of intracellular digestion

1. phagocytic cells take up bacteria 2. delivers it to lysosome = fusion 3. formation of phagolysosome 4. breakdown and release of reactive oxygen species 5. microbes are killed

mechanisms of microbial evasion

inhibition of adherence (M protein, capsules) kill phagocytes (leukocidins) lyse phagocytes (MAC) escape phagosomes prevent phagosome and lysosome fusion grow in phagolysosome

inflammation

innate -- nonspecific response to tissue injury caused by pathogen or trauma release of mediators to control

cardinal signs of inflammation

``` redness warmth pain swelling altered function ```

pyrogenic response

Fever caused by endotoxin release and phagocytotic induction of IL-1 IL-1 stimulates hypothalamus to release prostaglandins and raise temperature IL-1 is removed and body temps decline

advantages of fever

t cell production (due to IL-1) increase transferrins speed up repair process

disadvantages of fever

acidosis (via increased metabolic rate) dehydration tachycardia death

chemicals released by damaged cells

histamine kinins leukotreinces prostaglandins

histamine

vasodilation increases permeability of blood vessels this is why we take anti histamines

prostaglandins

intensity of histamine and kinin effect vasodilation and increased BV permeability