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Phase 1 > Ch. 1 Inflammatory Response > Flashcards

Ch. 1 Inflammatory Response Flashcards

1
Q

What are the macroscopic signs of acute infllamtion

A

rubor
calor
dolor
tumor

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2
Q

What induces vasoconstriction immediately upon injury

A

catecholamines
serotonin
bradykinin
prostaglandins

all released from local tissues

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3
Q

what induces vasodilation

A
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3
Q

what induces vasodilation

A

vascular smooth muscle changes that are mediated by nitric oxide, histamine, leukotrienes, prostaglandins, and complement factors

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4
Q

how is permeability of vasodilation mediated?

A

histamine and serotonin mediate an increase in the number and size of intracellular endothelial gaps in the venules called transcytoplasmic channels or vesiculovacuolar organelles
Interendothelial gaps also form

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5
Q

Why does edema occur in early inflammation

A

increased permeability = serum protein loss = decreased intravascular osmotic pressure and increased blood viscosity –> inreases in hydrostatic pressure means edema fluid accumulation

Edema is advantageous because it facilitates delivery of antibodies and acute phase proteins to the site of inflammation

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6
Q

What is Sialyl Lewis X complex

A

weak transient interactions between selectins (glycoprotein cell adhesion molecules on endothelial cells) and ligands their leukocytes occur
Sialyl Lewis X is one with a carbohydrate ligand

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7
Q

What are the three most commonly described endothelial selectins?

A

E, P, and L selectins

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8
Q

What are integrins

A

proteins on the leukocytes that have alpha (CD11a, CD11b, CD11c) and beta (CD18) subunits that bind to corresponding proteins on the endothelium

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9
Q

What does Integrin ligand ICAM-1 interact with

A

interacts with integrins called lymphocyte associated antigen 1 (LFA-1 which is also CD11a/CD18) and macrophage antigen 1 (Mac 1 which is also known as CD11b/CD18)

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10
Q

How does diapedesis occur

A
  • adhesion molecules like ICAM 1 is expressed more near interendothelial junctions and facilitate migration
  • platelet endothelial cell adhesion molecules like PECAM 1 also facilitate leukocyte transendothelial migration and transmigration through the basement membrane
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11
Q

What are the four processes of acute vascular response

A

vasodilation
increased permeability
stasis
leukocyte extravasation

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12
Q

How do neutrophils kill bacteria

A

phagocytosis
release of superoxide radicals
formation of neutrophil extracellular traps

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13
Q

what are neutrophil extracellular traps

A

cell free DNA and other antimicrobial peptides including histones ensure a local high concentration of granule enzymes

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14
Q

WHat is azurophil

A

this is the primary neutrophil granule

contains microbicidal polypeptides such as myeloperoxidase, defensins, lysosome hydrolases, neutral proteases

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15
Q

what are examples of secondary neutrophil granules

A

metalloproteases

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16
Q

what are examples of tertiary neutrophil granules

A

gelatinase

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17
Q

what are the primary cytokines released by neutrophils

A

Interleukin 1 alpha - IL-1a
Interleukin 1 beta - IL-1b
interleukin 6 - IL-6
tumor necrosis factor alpha - TNF a

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18
Q

How do neutrophils go from a resting state to primed

A

two stage process
within minutes of stimulation by bacterial products or cyto/chemokines, mobilization of tertiary granules and secretory vesicles increase neutrophil cell surface receptors

At the same time, new expression of receptors and cytokines are induced

This allows primed neutrophils to release reactive oxygen species and other inflammatory mediators as well as increase their life span

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19
Q

What chemical signals will macrophages respond to to cause extravasation

A 
fibronectin
elastin
complment factors C3a and C5a
thrombin
PDGF
TGF beta (transforming growth factor)
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20
Q

What is the main macrophage type in inflammatory conditions

A

monocyte derived macrophages (remember, macrophages either come from monocytes or they start as tissue resident marophages)

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21
Q

What is macrophage polarization

A

macrophages will assume two functional phenotypes: M1 or M2

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22
Q

Describe the characteristics of M1 macrophages

A

activated by infectious agents or proinflammatory cytokines like interferon gamma (IFN-y) or TNF alpha
Debride the affected site by phagocytosis
Secrete IL-1b, IL-6, TNF alpha, prostaglandins
secrete collagenases and elastases

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23
Q

Describe the characteristics of M2 macrophages

A

activated in response to ANTI inflammatory cytokines like IL4, IL13, IL10
aid in wound repair and healing by releasing PDGF and TGF beta
secrete collagenases and elastases

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24
Q

Toll like receptors, scavenger receptors, mannose receptors, c type lectin like domain containing receptors, peptidoglycan recognition receptors and nucleotide binding site leucine rich repeat receptors are all part of what group

A

pattern recognition receptors, many will bind to more than one alarm signal molecule

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25
Q

What does toll like receptor 4 (TLR4) respond to?

A

it is a major receptor for lipopolysaccharide, an endotoxin
in concert with receptor CD14, TLR4 will activate expression of numerous proinflammatory mediators and expression of more TLRs

Responds to the following PAMP/DAMP: lipopolysaccharide, mannan, heparan sulfate, heat shock protein 60

26
Q

what is nuclear factor kappa B?

A

NF-κB is one of the main type 1 transmembrane proteins that alter gene expression to lead to more reactive oxygen species, NO, and eicosanoids. It is activated in a macrophage wtih TLR activation

27
Q

The same cytokine may act at different receptors and the same receptor may accept multiple cytokines. This is a promiscuity in receptor affinity. What is the benefit?

A

ensures the maintenance of innate immune responses

28
Q

What are PAMPs/DAMPs

A

pathogen associated molecular patterns or

danger associated molecular patterns

29
Q

What DAMPs/PAMPs does TLR 2 respond to

A

toll like receptor 2 responds to:

  • lipoproteins
  • lipopolysaccharides
  • heat shock protein 70
30
Q

What is the archetypal neutrophil chemoattractant

A

the chemokine IL 8 which is also known as CXCL 8
will attract neutrophils but also upregulates surface adhesion molecules, triggers degranulation of proteases, increases the production of other inflammatory mediators

31
Q

How does interleukin 10 act as an anti inflammatory cytokine

A
  • inhibits NF-κB which decreases response to TNFa, IL1, IL6, IL8
  • degrades mRNA
  • downregulates Th-1 helper t cell cytokine production
  • promotes shedding of TNF receptors
  • inhibits antigen presentation

IL 10 is mostly produced by CD4 Th-2 helper cells, monocytes, and B cells

32
Q

What is the cell origin and physiologic action of PGE2

A

many cell types produce it

causes hyperalgesia, potent pyrogenic agent, vasodilation, increases proresolution molecules

33
Q

What is the cell origin and physiologic action of PGD2

A

Produced by mast cells and causes vasodilation, chemoattractant, increases proresolution molecules, and causes bronchoconstriction

34
Q

What is the cell origin and physiologic action of PGF2alpha

A

produced by endometrial cells and stimulates uterine contraction, bronchoconstriction, and vasodilation

35
Q

what is the cell origin of PGI2 (prostacyclin) and physiologic action

A

produced by endothelial cells and causes vasodilation, inhibits platelet aggregation, and causes hyperalgesia

36
Q

What is the cell origin of TxA2 (thromboxane) and its physiologic action

A

released by platelets and macrophages and causes platelet aggregation and vasoconstriction

37
Q

How do proresolution eicosanoids act?

A

halt neutrophil infiltration
activate macrophage phagocytosis
increase clearance of phagocyts
stimulate expression of molecules involved in anti microbial defense like the lipoxins

38
Q

What is lipoxin

A
  • a molecule involved in antimicrobial defense
  • produced by a transcellular biosynthetic mechanism requiring cell to cell interactions to metabolize arachidonic acid
  • Aspirin actually increases the production of some lipozins
  • lipoxins block secretion of TNFa from T cells
  • inhibit leukotriene induced neutrophil chemotaxis by blocking Beta 2 integrin mediated cell adhesion and decreasing P selectin expression -
39
Q

How are fish oils anti inflammatory

A

contain eicosapentaenoic and docosahexaenoic acid which are the precursors for resolvins and protectins (two proresolution mediators) and those then bind to g protein coupled receptors on leukocytes
Eicosapentaenoic acid is also a competitive inhibitor to arachidonic acid

40
Q

What are the functions of platelet activating factor

A
  • stimulates arachidonic acid release by binding to g protein coupled receptors
  • increases affitiny and avidity of surface integrins
  • increases platelet aggregation and degranulation
  • increases eosinphil degranulation
  • increases reactive oxygen species production
  • increases vascular permeability, bronchoconstriction, pulmonary vasoconstriction
41
Q

What degrades platelet activating factor

A

platelet activating factor acetylhydrolase

42
Q

What is frustrated phagocytosis

A

a phagocyte fails to engulf its target and releases damaging agents

43
Q

What is redox signalling?

A

non phagocytic cells produce H2O2 in the wound bed and that promotes keratinocyte migration and proliferation

44
Q

What does carbon monoxide do in the inflammatory process?

A

has antiinflammatory effects that impair the production, differentiation, and activation of inflammatory cells

45
Q

WHat is the role of IL 12

A

serum amyloid A increases IL 12 production which is needed for Th1 cell antimicrobial response

46
Q

What is the role of IL 23

A

increased in response to serum amyloid A, will play a role in chronic and autoimmune inflammation in monocytes

47
Q

How is the classical complement pathway activated?

A

immune complexes activate the classical pathway

48
Q

how is the lectin complement pathway activated

A

Via interaction of hepatically synthesized lectin proteins with surface carbohydrates on pathogens

49
Q

How is the alternative complement pathway activated

A

contact with foreign microbes

50
Q

All three pathways of the complement factors converge to cleave C3 to C3a and C3b, what happens to C3b?

A

C3b will bind to either classical C3 convertase (C4bC2a) or alternative C3 convertase (C3bBb)

51
Q

What do classical C3 convertase (C4bC2a) and alternative C3 convertase (C3bBb) do?

A

Cleave C5 to C5a and C5b

52
Q

What is C5b’s role in the complement cascade?

A

Binds to C6, C7, zc8, and C9 in the terminal complement pathway to make the membrane attack complex

53
Q

What does the membrane attack complex do?

A

inserts into the lipid bilayer of target cell membranes and creates channels, leading to dysregulation of cellular homeostasis and eventual lysis
This will destroy intracellular pathogens but it will also lead to tissue destruction

54
Q

What do C3a, C4a, and C5a have in common

A

they are anaphylatoxins that are cleavage products on the complement cascade
they enhance leukocyte chemotaxis, inflammation and oxygen free radicals

55
Q

Which complement cleavage product is an activator of eosinophils and mast cells and suppresses the release of IL 6 and TNFa from B cells to decrease the antibody response

A

C3a

56
Q

What are opsonins?

A

phagocytosis by monocytes and neutrophils is enhanced with opsonins
the C opsonins coat target cells and allow for direct interaction and ingestion by phagocytes

57
Q

What are bradykinin 2 receptors known for?

A

B2 receptors are ubiquitously and constitutively expressed in healthy tissue

58
Q

What are bradykinin 1 receptors known for?

A

B1 receptors are produced in pathologic conditions

Production may be influenced by NF-κB

59
Q

What does bradykinin do?

A
  • mediator of endothelial prostacyclin synthesis, superoxide formation, and tissue plasminogen activator release
  • facilitates migration of polymorphonuclear leukocytes and stimulates cytokine synthesis
  • stimulates venous dilation through local NO releases, increases vascular permeability, produces pain response
  • inactivated by kininase
60
Q

What are some theories for the cause of multiple organ failure

A
  • reperfusion mediated oxidative injury to the gut epithelium
  • two-hit phenomenon - the initial event primes neutrophils and macrophages for an exaggerated response to subsequent events like secondary infection or prolonged hypotension
61
Q

endotoxin tolerance

A

a cell exposed to endotoxin becomes unresponsive to subsequent stimulation
most commonly recognized in monocytes/macrophages possibly due to reprogramming to downregulate inflammatory genes

62
Q

What is cross tolerance

A

exposure to another stimulus such as lipoteichoic acid from gram positive bacteria leaves the cell unresponsive to endotoxin

63
Q

How are fibroblasts involved in chronic inflammation

A 
Express CXCL8 (IL-8), CXCL12 (stromal cell derived factor or SDF-1), and CCL2 (monocyte chemoattractant protein MCP-1) 
Express CD40 receptor which engages with T cells and promotes expression of IL-6 and COX 2
Differentiates into myofibroblasts and that increases extracellular matrix like collagen and that leads to tissue fibrosis and sometimes granulomatous inflammation

Phase 1 (35 decks)

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