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MIIM30002 > Lecture 4: Innate Responses to Infection: Phagocytes > Flashcards

Lecture 4: Innate Responses to Infection: Phagocytes Flashcards

1
Q

What are macrophages derived from?

A

derived from the myeloid progenitor and mature continuously from blood monocytes

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2
Q

What is the role of macrophages?

A

carry out phagocytosis and inflammatory response signalling

important role in adaptive immunity

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3
Q

How do macrophages detect pathogens?

A

using pattern recognition receptors e.g. bacteria to mannose receptors

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4
Q

What happens during phagocytosis after the pathogen becomes bound to PRRs on the cell surface?

A

the pathogen is engulfed into the cell by the process of endocytosis into a phagosome, it fuses with a lysosome to form a phagolysosome and the bacterium is completely degraded

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5
Q

What do phagocytes present to the adaptive immune cells?

A

peptide fragments of broken down pathogens

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6
Q

How do phagocytes break down pathogens?

A

acidification, toxic oxygen-derived products, toxic nitrogen oxides, antimicrobial peptides, enzymes and competitors

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7
Q

What is respiratory burst?

A

when phagosome fuses with lysosome, NADPH-dependent oxidases generate toxic oxygen radicals and hydrogen peroxide (H2O2) -> accompanied by transient increase in O2 consumption

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8
Q

Why do activated phagocytes also produce nitric oxide?

A

NO reacts with oxygen radicals to produce peroxynitrite (ONOO-) -> damages molecules including DNA

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9
Q

Why aren’t our own cells also damaged by respiratory burst?

A

this process is accompanied by synthesis of enzymes to inactivate the damaging molecules e.g. superoxide dismutase converts superoxide to hydrogen peroxide and catalase converts H2O2 to water and O2

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10
Q

What induces the synthesis of inflammatory cytokines in macorphages?

A

binding of bacterial components to signalling receptors

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11
Q

What do cytokines produced by macrophages cause?

A

dilation of local small blood vessels

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12
Q

What are cytokines? How do they act on cells?

A

small glycoproteins that mediate immune cell communication and act by binding to specific receptors on cells

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13
Q

What happens if there are defects in cytokine production, signalling or regulation?

A

this can lead to autoimmunity (e.g. inflammatory disease)

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14
Q

How do autocrine, paracrine and endocrine cytokines act?

A

autocrine: affect the behaviour of the same cell
paracrine: affect the behaviour of a local cell
endocrine: affect the behaviour of a distant cell

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15
Q

What do chemokines regulate?

A

the movement of cells

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16
Q

What is the role of IL-1B?

A

activates vascular endothelium
activates lymphocytes
local tissue destruction
increases access of effector cells

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17
Q

What is the role of TNF-a

A

activates vascular endothelium and increases vascular permeability, which leads to increased entry of IgG, complement, and cells to tissues and increased fluid drainage to lymph nodes

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18
Q

What is the role of IL-6

A

lymphocyte activation

increased antibody production

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19
Q

What is the role of IL-8

A

chemotactic factor recruits neutrophils, basophils, and T cells to site of infection

20
Q

What is the role of IL-12

A

activates NK cells

induces the differentiation of CD4 T cells into Th1 cells

21
Q

What are acute phase proteins?

A

proteins produced by the liver and released into circulation

22
Q

How does plasma concentration of acute phase proteins differ in the absence of infection and within a day or two of infection?

A

in the absence of infection plasma concentration is very low and within a day or two of infection plasma concentration rises very quickly

23
Q

What is the synthesis and release of acute phase proteins stimulated by?

A

inflammatory cytokines

24
Q

What are some examples of acute phase proteins?

A

CRP and mannose-binding lectin

25
Q

What is the role of CRP?

A

binds phosphocholine on bacterial surfaces, acting as an opsonin and as a complement activator

26
Q

What is the role of mannose-binding lectin?

A

binds to carbohydrates on bacterial surfaces, acting as an opsonin and as a complement activator

27
Q

What is CRP an indicator of?

A

inflammation

28
Q

What are neutrophils derived from and where are they stored?

A

derived from the myeloid progenitor and stored in bone marrow -> released progressively in steady state

29
Q

Are macrophages or neutrophils terminally differentiated in bone marrow?

A

neutrophils

30
Q

What is the role of neutrophils?

A

move in large numbers to sites of infection (cytokine stimulation) so that they can carry out phagocytosis and form NETs

31
Q

Are macrophages or neutrophils short lived?

A

neutrophils

32
Q

How do cytokines direct neutrophil migration?

A

induce higher expression of adhesion molecules and stronger interactions

33
Q

How do neutrophils migrate?

A

bind to endothelium and squeeze between cells -> enter infected tissue and make up the first wave of cells that cross the blood vessel wall to enter and inflamed tissue

34
Q

What allows leukocytes to roll along the vascular endothelial surface?

A

selectin-mediated adhesion to leukocyte sialyl-Lewis^x is weak

35
Q

What is the process by which neutrophils enter into the site of infection?

A

rolling adhesion -> tight binding -> diapedesis -> migration

36
Q

What are some examples of adhesion molecules?

A

LFAs: leukocyte functional antigen
ICAMs: intercellular adhesion molecules

37
Q

How does rolling adhesion occur?

A

selectin is transported to surface of the endothelium after exposure to inflammatory mediators -> selectins bind to the S-LEx carbohydrate ligand on the neutrophil allowing adherence to endothelium -> reversible reactions allow neutrophils to “roll”, or be forming and breaking new adhesive interactions

38
Q

How does tight binding occur?

A

interaction of the LFA-1 on neutrophil and adhesion molecules on endothelium (ICAM-1) -> exposure to chemokine (CXCL8) released by stimulated macrophages promotes conformation change to strengthen the adhesion (strongly induces expression of ICAM-1) -> neutrophil stops rolling and tightly binds to endothelium

39
Q

How does diapedesis occurs?

A

neutrophil crosses blood vessel wall by squeezing between cells (extravasation) -> proteases (such as elastase) secreted by neutrophil break down basement membrane

40
Q

How does migration occur?

A

neutrophil migrates towards centre of infection following concentration gradient (CXCL8/IL-8 and TNF-a)

41
Q

How do neutrophils undergo phagocytosis?

A

neutrophils express receptors for many bacterial and fungal constituents -> neutrophils bind bacteria, engulf them, and destroy them with the toxic contents of the neutrophil granules -> they quickly die after phagocytosis and degradation of the pathogen -> build-up of dead neutrophils at site of infection leads to the formation of pus

42
Q

What is fMet-Leu-Phe?

A

bacterial tri-peptide released by bacteria (with formylated Met)

  • > chemotactic factor
  • > activator of phagocytosis / degradation
43
Q

How do neutrophils kill microbes apart from phagocytosis?

A

neutrophils use a novel mechanism of destruction that is directed at extracellular pathogens

44
Q

How are NETs formed?

A

neutrophil undergoes cell death (NETosis), the nuclear chromatin is released into extracellular space and forms a fibril matrix know as NETs

45
Q

How do NETs kill?

A

capture microorganisms and work to increase pathogen clearance by increasing the efficiency of phagocytosis by neutrophils or macrophages

MIIM30002 (25 decks)

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