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BMS150 > INNATE IMMUNOLOGY AND INFLAMMATION > Flashcards

INNATE IMMUNOLOGY AND INFLAMMATION Flashcards

lecture 2

1
Q

what are lysozyme chemical barriers?

A

present in secretions and use hydrolysis to break proteoglycan wall of bacteria cell wall

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2
Q

what are defensins?

A

small, hetergeneous, cationic, antimicrobial peptides (chemical barrier)

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3
Q

what do defensins do?

A
  • chemical barrier
  • destabilizes membranes and pore formation in bacterial cell walls
  • proteolytic degradation of bacterial proteins
  • inhibit viral binding and entry
  • inhibit virus particle assemble
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4
Q

where are defensins stored?

A

neutrophil granules and secreted by epithelial cells

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5
Q

how do defensins kill microbes?

A

extracellularly –> released when neutrophils die during inflammation
intracellularly –> after a cell phagocytoses a pathogen

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6
Q

what are the major phagocytes in the body?

A

macrophages and neutrophils

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7
Q

monocytes –> macrophages

A

pro-monocytes –> monocytes –> macrophage/ macrophage like cells

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8
Q

are macrophages long or short lived?

A

long lived

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9
Q

what are neutrophils?

A

non-dividing, short lived cells derived from hematopoietic precursors in the bone marrow

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10
Q

what is pattern recognition?

A

immediate recognition for common ‘signs’ of microbial infection

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11
Q

what are PRRs

A

pattern recognition receptors found on phagocytes in response to PAMPs or DAMPs

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12
Q

what are some examples of PRRs?

A

toll-like receptors, nod-like receptors, lectins

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13
Q

what responses do PRRs elicit?

A

phagocytosis and cytokine secretion

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14
Q

what are the steps of phagocytosis?

A
  1. PRR binds to a microbe
  2. microbe is engulfed by phagocyte –> forms a phagosome
  3. microbe killing –> use molecules like ROS, pore forming proteins, hydrolytic enzymes, pH changes
  4. microbe remnants are digested and used, or excreted
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15
Q

what is a common way for macrophages to kill cells

A

by synthesizing nitric oxide

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16
Q

how do neutrophils kill cells?

A

use pore-forming molecules within their granules

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17
Q

what are some neutrophil granules?

A

defensins, cathepsin, cathelicidins, lysosomes, lactoferrin

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18
Q

what are cathepsin?

A

a type of protease

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19
Q

what are cathelicidins?

A

pore forming molecule –> cause lysis

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20
Q

what are lysozymes?

A

glycoside hydrolase

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21
Q

what granule is best at killing gram +(ve) bacteria

A

lysozymes

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22
Q

what are lactoferrin?

A

iron binding protein that interferes with iron metabolism in microbes

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23
Q

what are NETs

A

in environments with lots of bacteria, neutrophils can lyse and release their DNA into the ECF

24
Q

what do NETs do?

A

trap bacteria because they’re sticky and hold them to chromatin –> histones are toxic to many bacteria

25
Q

what are toll like receptors?

A

transmembrane receptors that make cytokines

26
Q

what inflammatory cytokines do TLRs secrete

A

inflammatory cytokines (IL-1beta, IL-6, CXCL8, IL-12, TNFalpha)

27
Q

what interferons are secreted by TLRs

A

IFN alpha, beta, and lambda –> can activate macrophages, NK cells, and inducing antiviral state

28
Q

what is MyD88?

A

essential adaptor in TLR signaling

29
Q

what is a MyD88 deficiency?

A

suffer severe bacterial infections but antiviral responses are unaffected

30
Q

what happens when MyD88 is too active?

A

can develop various blood disorders and cancer because of over production of IgM

31
Q

what are nod like receptors?

A

intracellular receptors found in cytoplasm

32
Q

what is the main goal of NLRs?

A

increase cytokine production, recognize DAMP

33
Q

what is the first step in acute inflammation?

A
  • vasodilation: increases blood flow at capillary bed
34
Q

what is used to induce vasodilation?

A

nitric oxide, histamine, prostaglandins, platelet activating factor, complement (C5a and C3a)

35
Q

how does nitric oxide effect vasodilation?

A

potent vasodilator at low concentrations, at high concentrations it can kill microbes and host cells

36
Q

what is vascular congestion?

A

vasodilation and fluid loss due to increased permeability lead to slower blood flow –> helps margination of leukocytes

37
Q

what is chemotaxis?

A

tells the cell which direction to go to

38
Q

what are important prostaglandins for vasodilation?

A

PGE2, PGD2, PGI2

39
Q

how are the prostaglandins and leukotrienes for vasodilation produced?

A

when PLA2 generates arachidonic acid from membrane phospholipids

40
Q

what is LTB4

A

important chemotactic agent

41
Q

what are lipoxins?

A

generated from arachidonic acid by 12 lipoxygenase to decrease inflammation

42
Q

what is the second step in acute inflammation?

A

enhancement of vascular permeability –> capillaries and venules become more leaky because of a number of mediators

43
Q

what mediators enhance vascular permeability

A

histamine and serotonin, prostaglandins (PGD2, PGE2), leukotrienes (LTC4, LTD4, LTE4), platelet activating factor, C3a, C5a, bradykinin

44
Q

what increases vascular permeability?

A

contraction of endothelial cells, endothelial damage , transcytosis

44
Q

what is lymphatics?

A

fluid accumulation during inflammation

45
Q

what is transcytosis?

A

used to quickly transport antibodies (problem if it occurs accidentally)

46
Q

what is lymphangitis?

A

when lymphatic vessels become inflamed

47
Q

what is the 3rd step in acute inflammation?

A

emigration and activation of leukocytes

48
Q

what leukocytes emigrate to site of incident during acute inflammation?

A

neutrophils, monocytes, eosinophils, basophils

49
Q

what are the steps to leukocyte migration during acute inflammation?

A

margination, rolling, adhesion, diapedesis, chemotaxis of leukocytes to site of injury

50
Q

what are the two different chemokine families?

A

CXC and CC

51
Q

what are CXC?

A

chemokines that attract neutrophils

52
Q

what are CC

A

chemokines that act on a variety of other leukocytes

53
Q

what are chemokines?

A

small cytokines that bind to cell-surface receptors and induce movement of leukocytes along chemokine concentration gradient

54
Q

what are E and P selectin used for?

A

present on endothelium and bind to white blood cells and are responsible for rolling

55
Q

what is responsible for tight binding during the emigration stage of acute inflammation?

A

integrins: LFA-1, MAC-1, VLAS-4, alpha4beta7
TNF and IL1 and chemokines

56
Q

what agents are produced in higher concentrations on sites of injury?

A

leukotriene B4, N-formyl-methionine, C5a, chemokines

BMS150 (5 decks)

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