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MFMII > Innate Immunity I > Flashcards

Innate Immunity I Flashcards

1
Q

main function of the skin

A

prevent colonization of microbes

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2
Q

main methods that epithelial cells use as physical barriers

A
  1. tight junctions
  2. stratum corneum
  3. mucus
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3
Q

how do tight junction in epithelial cells?

A

block microbial passage

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4
Q

how does stratum corneum help as a physical barrier?

A

outer layer of skin flakes off and thereby removes adherent microbes

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5
Q

how does mucus help as a physical barrier?

A

captures pathogens and foreign agents and then is removed by ciliary action in the bronchial tree and sneezing and coughing, also peristalsis of gut, vomiting and diarrhea in GI tract

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6
Q

what are defensins?

A

antimicrobial peptides rich in Arg with both hydrophobic and hydrophilic regions

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7
Q

where are defensins made?

A

paneth cells in the gut, neutrophils and epithelial cells

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8
Q

how do defensins act?

A

insert into microbial membranes, make pores, fluid leaves microbe and it lysis

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9
Q

in which environment do defensins act best?

A

sweat, tears, gut lumen, phagosome – not well in physiological conditions

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10
Q

how is mucosal microbiota level controlled?

A

defensins are constitutively secreted to maintain levels of microbiota

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11
Q

what are pentraxins?

A

cyclic proteins that circulate in blood and lymph, bind to pathogen surfaces, and serve as target site for phagocyte attachment (aka docking site for neutrophil or macrophage)

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12
Q

what occurs upon binding of phagocytes to pentraxin+pathogen?

A

phagocyte engulf and destroy attached pathogen

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13
Q

what are the short pentraxins?

A
  1. c reactive protein CRP

2. serum amyloid P SAP

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14
Q

how are short pentraxins induced?

A
  1. IL-6 is released in response to microbes and tissue damage
  2. IL-6 binds to hepatocytes and stimulates release of CRP and SAP
    IS A SYSTEMIC RESPONSE
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15
Q

what are the long pentraxins?

A

pentraxin 3 (PTX3)

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16
Q

how is PTX3 induced?

A
  1. infiltrating DC, macrophage, EC, and PMN sense microbes and tissue damage
  2. infiltrating cells release PTX3 as a local response
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17
Q

where are lysozymes found

A
  1. saliva
  2. tears
  3. mucus
  4. plasma
  5. tissue fluids
  6. phagocytic granules (neutrophil granules)
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18
Q

what do lysozymes do?

A

hydrolyze 1,4 beta linkages between bacterial wall peptidoglycan NAG and NAM, increasing permeability and causing bacteria to burst

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19
Q

describe bacterial wall peptidoglycan

A

repeating amino sugars N-acetylglucosamine (NAG) and N acetylmuramic acid (NAM) which are linked by 1,4 beta linkages, and then crosslinked by peptide bridges

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20
Q

what makes peptide bridges of peptidoglycan?

A

transpeptidase

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21
Q

which antibiotic targets transpeptidase?

A

penicillin

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22
Q

which are chemical barriers used in innate immunity?

A
  1. defensins
  2. pentraxins
  3. lysozyme
  4. phospholipase A2
  5. cathelicidins
  6. lactic and fatty acids
  7. lactoferrin and transferrin
  8. hydrochloric acid
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23
Q

what does phospholipase A2 do

A

penetrates bacterial cell wall and hydrolyzes membrane phospholipids

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24
Q

what do cathelicidins do?

A

form membrane disrupting proteins that are specific to bacteria

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25
Q

where are cathelicidins release?

A

released by skin and mucosal epithelial cells, they are cleaved into toxic peptides by bacteria

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26
Q

what do lactic acid and fatty acids do?

A

found in perspiration and oily secretions and inhibit bacterial growth due to decreased pH

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27
Q

where is transferrin and lactoferrin found?

A

body secretions, plasma and tissue fluid

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28
Q

what do lactoferrin and transferrin do for immunity?

A

sequester iron for use by human cells only and not bacteria

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29
Q

what does HCl do?

A

gastric secretions destroy bacterial membranes (swallowed)

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30
Q

what does UREA do?

A

disrupts cell membranes

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31
Q

unique characteristics of babies at birth

A

before birth, babies have no commensal microbes, but upon birth, contact with vagina makes skin and mucosal surface begin to colonize

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32
Q

how are microbiota used as a barrier?

A

pathogens must compete with the existing body microbiota (which are well adapted) for nutrients and space

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33
Q

where is the highest density of bacteria found?

A

large intestine (area of lowest oxygen concentration)

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34
Q

what are 3 events that lower microbiome diversity?

A
  1. western diet high in saturated fat, high sugar, and low fiber
  2. aging
  3. reduction in physical activity
  4. chronic stress
35
Q

describe the change of the microbiome with development

A
  1. at birth, only enterobacteriaceae
  2. up until 2-3 years, microbiota grow and diversify
  3. 2-3 years old, bacteroidacea (anaerobe) should be the most plentiful microbiota
36
Q

what is the first line of defense against harmful agents?

A

after (skin)

gut epithelium bc 80% of immune cells reside there

37
Q

how does chronic stress impact microbiota?

A
  1. lowers mucus producing goblet cells and MUC2 mRNA (thins/impairs mucus production)
  2. increases mucolytic bacteria (further thinning mucus layer)
  3. expansion of bacteria and loss of mucus triggered immune reactivity
  4. chronic inflammation –> intestinal damage, colitis
38
Q

what does MUC2 do?

A

MAJOR COMPONENT OF MUCUS IN COLON encodes for mucin, which is secreted continuously to refill the inner mucus layer from underneath. the inner layer of mucus keeps bacteria at a distance from the epithelial cell

39
Q

what is complement?

A

collection of 30+ proteins made by the liver (constitutively), present in blood, lymph, extracellular fluid

40
Q

when is complement activated?

A

as soon as pathogen penetrates epithelial barrier

41
Q

what do complement proteins do?

A

coat bacterial surface and extracellular viral particles to make them more easily phagocytosed

42
Q

how are complement proteins made?

A

made in liver as zymogens that must be cleaved to be activated

43
Q

3 functions of complement activation (high yield)

A
  1. microbial lysis
  2. inflammation (accentuates or triggers)
  3. enhanced phagocytosis aka opsonization (binding site for phagocytes to grab bacteria)
44
Q

describe release of complement protein 3 (C3)

A
  1. C3 released from liver in inactive form
  2. water hydrolyzes C3 (or spontaneous conformation change) exposing nucleophile (thioester bond) for nucleophile attack INTO C3b AND C3a
  3. nucleophile attacks pathogen
45
Q

why does C3 have a thioester bond?

A

allows for binding to hydroxyl or AA side chain or glycoproteins on pathogen; ensures that C3b binds to surface of microbe

46
Q

describe the nucleophilic attack of C3

A

can occur by water (most often) or amino group NH2/hydroxyl OH groups of protein/carbs on pathogen surface

47
Q

can C3b attack the body’s own cells

A

yes, so there is inhibitory systeems in our cells to prevent complement fixation/activation on self cells

48
Q

what is complement fixation?

A

the attaching of C3b and the pathogen’s carbs/protein surface

49
Q

what would occur if there was a deficiency in the complement system?

A

recurrent infections of encapsulated microbes like strep, staph, multiple occurrences of meningitis or pharyngitis (neisseria)

50
Q

generalized mechanism of the complement

A

places handles on the microbes so phagocytes can attach, especially important for bacteria that are encapsulated

51
Q

describe the alternate pathway (before it attaches to pathogen surface)

A
  1. C3 undergoes spontaneous change in the aqueous environment of tissues/blood
  2. C3’s exposed thioester bond attaches to H2O making iC3 (inactive C3)
  3. the amount of iC3 increases near surface of pathogen but not attached
  4. iC3 binds factor B
  5. iC3 bound factor B is cleaved by factor D
  6. Ba is released, Bb is bound to iC3
  7. C3 convertase (iC3Bb) cleaves C3
  8. C3a is released, C3b attaches to pathogen surface
52
Q

describe the alternate pathway (once it is already attached to surface)

A
  1. pathogen bound C3b binds factor B again and promotes cleavage by factor D
  2. cleavage by factor D makes C3bBb (C3 convertase)
  3. more C3bBb can then make more C3b
  4. C3b rapidly accumulates on pathogen surface
53
Q

what is C3bBb?

A

potent C3 convertase

54
Q

what does properdin do?

A

Factor P, enhances alternative C3 convertase activity (aka stabilizes C3 convertase complex and prevents degradation)

55
Q

what does factor H do?

A
  1. binds to C3b together with factor I and inactivates C3b (makes iC3b which cannot form C3 convertase or bind to surface)
  2. accelerates decay of C3bBb
56
Q

what occurs with a deficiency of factor I

A

factor H cannot inactivate C3bBb or C3b. C3bBb is unchecked, C3 is depleted, and human cells are more susceptible to infections by encapsulated bacteria (ear infection, abcesses)

57
Q

which factors block complement activation on human cells?

A
  1. Delay accelerating factor (DAF)
  2. membrane cofactor protein (MCP)
  3. factor H binds to sialic acid on human cells and recruit Factor I
58
Q

what does DAF do

A

binds to C3b and dissociates Bb to inactivate C3 convertase

59
Q

what does MCP do

A

binds to C3b and recruits factor I for the cleavage of C3b to iC3b

60
Q

what bacteria use sialic acid to inactivate complement?

A
  1. streptococcus pyogenes

2. staphylococcus aureus

61
Q

what are the first cells that a pathogen encounters upon invasion?

A

tissue resident macrophages (so they can produce cytokines and respond to complement)

62
Q

where are macrophages found?

A
  1. connective tissue
  2. lining of GI tract
  3. lining of respiratory tract
  4. Kupffer cells in liver
  5. microglia in brain
  6. alveoli of lung
63
Q

lifespan of resident macrophages?

A

long lived phagocytic cells

64
Q

when would macrophage number be increased?

A

where there is a lot of dead cells to be cleared out

65
Q

describe the function of complement activation

A
  1. macrophages express complement receptors that enhance phagocytosis
  2. C5b initiates formation of membrane attack complex (MAC) for lysis
  3. C3a and C5a promote inflammation
66
Q

what occurs once complement is activated?

A

deposition of C3b on the bacterial cell surface, where the complement receptor 1 (CR1) on the macrophage can bind to the fragments of C3b on pathogen

67
Q

what does complement receptor 1 do?

A
  1. it is a receptor on macrophages that binds C3b on bacterium
  2. disrupts C3 convertase, prevents C3b being added to the macrophage itself
68
Q

what is opsonization?

A

facilitated phagocytosis by receptor-ligand interactions

69
Q

describe the events after complement is activated?

A
  1. complement activation leads to deposition of C3b on bacterial cell surface
  2. CR1 on macrophages binds C3b on bacterium
  3. macrophage endocytoses the bacterium
  4. macrophage membranes fuse, creating a membrane bounded vesicle (phagosome)
  5. lysosomes fuse with phagosome forming a phagolysosome
70
Q

what initiates lysis of the bacterium?

A

C3b, by binding to alternative C3 convertase, makingn alternative C5 convertase aka C3b2Bb

71
Q

what is C5 convertase

A

C3b that bound to C3bBb to make C3b(squared)Bb; which is cleaved to C5a and C5b fragments

72
Q

what does C5b do?

A

initates formation of membrane attack complex (MAC)

73
Q

describe the formation of the Membrane Attack Complex (MAC)

A
  1. C5b binds to C6 = stable complex with binding site for C7
  2. C7 binds to C5bC6
  3. hydrophobic region of C7 is exposed for initial attachment to pathogen membrane
  4. C8 binds to C5bC6C7
  5. hydrophobic region of C8 is exposed that inserts into pathogen membrane, allowing C9 to form a pore
  6. C9 binds to C8 and assembles around it, spanning the membrane
  7. osmotic lysis occurs in the pathogen
74
Q

what factors block alternative C5 convertase in human cells?

A
  1. CD59 (protectin)

2. S protein

75
Q

how does CD59 and HRF (homologous restriction factor) block C5 convertase?

A

prevents recruitment of C9 monomers to the C5bC6C7C8 complex

76
Q

how does S protein (and clusterin and Factor J) block alternative C5 convertase?

A

prevents C7 interaction with the cell membrane

77
Q

what fragments promote inflammation?

A

C3a and C5a that were generated during complement activation

78
Q

how exactly does C3a and C5a promote inflammation?

A
  1. promotes degranulation of mast cells and basophils in tissues
  2. increases vascular permeability due to the released products of mast cells and basophils – loosens tight junctions on local blood vessels
  3. promotes vasodilation by histamine
  4. increases recruitment of neutrophils and monocytes from the blood to the site of inflammation
  5. increased complement receptor on phagocytes
  6. contraction of visceral smooth muscle
79
Q

what causes anaphylactic shock?

A

too much C3a and C5a causes widespread leakage and hemorrhage

80
Q

what does increased vascular permeability lead to?

A

edema and decreased blood pressure

81
Q

what does vasodilation and increased vascular permeability lead to?

A

decreased blood pressure, and tachycardia to compensate for lack of bloock, and ischemic shock due to lack of blood.

82
Q

what is the consequence of ischemia in the cells?

A

cells produce toxins from ATP production that kill the cell

83
Q

what does smooth muscle contraction lead to?

A

wheezing, dyspnea, asphyxiation

84
Q

what does increased gland secretion lead to ?

A

increased mucus, which leads to dyspnea

MFMII (29 decks)

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