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Infection And Immunity > Chemotaxis and Phagocyte Infiltration into tissue > Flashcards

Chemotaxis and Phagocyte Infiltration into tissue Flashcards

1
Q

define Chemotaxis

A

The movement of cells in response to a chemical stimulus

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2
Q

why is chemotaxis required?

A

Enables cells to accumulate where most needed

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3
Q

how does chemotaxis work?

A

Cell motility achieved by temporary attachment of
“front” of cell to a surface, and by the formation of
actin filaments which pull the back of the cell towards the front

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4
Q

in nature where does chemotaxis and killing occur?

A

in tissues

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5
Q

How do the leukocytes “know where to go”?

A

Signals release by damaged or infected tissues change the local blood vessels

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6
Q

what is a localized acute inflammatory response?

A

vasodilation, vascular permeability, leukocyte migration

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7
Q

what is the role of neutrophils

A 
central role (get there 1st)
attracted by IL-8 (CXCL8), C3a, C5a, Prostaglandins
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8
Q

whats the role of macrophages?

A

arrive 5-6 hr later,
attracted by CC chemokines, C3a, C5a
secrete IL-1, IL-6, IL-8 (CXCL8),TNF localized and systemic effects

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9
Q

name the 5 Groups of Chemical Mediators of Inflammation and Chemotaxis

A 
A) Cytokines
B) Plasma enzyme systems
C ) Vasoactive amines
D) Arachidonic acid metabolites
E ) Chemokines
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10
Q

which cells secrete cytokines?

A

activated macrophages

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11
Q

name 5 cytokines

A 
CXL8
IL-12
IL-6
IL-1b
TNF-a
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12
Q

describe the action of IL-1b

A

Activates vascular endothelium and lymphocytes
local tissue destruction
increases access of effector cells

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13
Q

describe the action of TNF-a

A
  • Activates vascular endothelium

- increases vascular permeability increasing entry of IgG, cells to tissues and fluid drainage to lymph nodes.

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14
Q

what are the systemic affects of IL-6, IL-1b and TNF-a?

A

IL-1b- fever and IL-6 production
TNF-a- Fever, mobilisation of metabolites and shock
IL-6- Fever and induces acute phase protein production.

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15
Q

what is the action of IL-6?

A
  • Lymphocyte activation

- increased Ab production

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16
Q

describe the action of CXCL8?

A

recruits neutrophils, basophils and T cells

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17
Q

describe the action of IL-12

A
  • activates NK cells,

- differentiate CD4 T cells into T helper cells.

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18
Q

what do Plasma Enzyme Systems do?

A

activates innate immune system even before microbes have entered or been detected

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19
Q

give an example of a Vasoactive amine

20
Q

what does Histamine do?

A
  • In granules of mast cells, basophils, platelets
  • Released by degranulation (triggered by C3a, C5a, etc.)
  • Promotes arteriolar dilation, smooth muscle contraction, and venular endothelial contraction,
  • Results in widening of interendothelial cell junctions with increased vascular permeability
  • Vascular actions similar to Bradykinin
21
Q

describe the action of Arachidonic Acid Metabolites

A
  • AA released from cell membrane by Phospholipases which have been activated by various stimuli and/or inflammatory mediators
  • AA metabolism occurs via two major enzyme pathways:
    lipoxygenase and cyclooxygenase
22
Q

name 3 Arachidonic Acid Metabolites in chemotaxis

A

prostaglandins, platelet activating factor and leukotriene b4

23
Q

whats the effect of prostaglandins?

A

increase vascular permeability
vascular dilation
neutrophil chemotaxis

24
Q

whats the effect of leukotriene B4?

A

neutrophil chemotaxis

25
Q

whats the effect of PAF?

A

platelet aggregation
eosinophil chemotaxis
neutrophil activation

26
Q

name 2 Important anti-inflammatory drugs that interact with the Phospholipid pathway

A

steroids and aspirin

27
Q

what does aspirin inhibit?

A

cyclooxyrgenase pathways

28
Q

what do steroids inhibit?

A

phospholipase

29
Q

what are Chemokines?

A

Small polypeptides, approx 100 amino acids in general, 7-16 kDa

30
Q

what are the Four families of chemokines?

A

CXC
CC
C
CX3C (fractalkine) 38 kDa

31
Q

what do Chemoattractant cytokines do?

A

Orchestrate leukocyte chemotaxis, adhesion, activation

32
Q

whats the structure of CC chemokines?

A

Two adjacent cysteine amino acids near start of protein

Bind to CC Receptors (CCRs)

33
Q

structure of CXC?

A

Have one amino acid (X) which separates the first 2 cysteines
Bind to CXC Receptors (CXCRs)

34
Q

name a CXC Chemokine

35
Q

whats the action of CC Chemokines?

A

Attract Monocytes not Neutrophils

36
Q

whats the action of TNF cytokines?

A

TNF causes Weibel-Palade bodies in endothelial cells to be secreted

Weibel -Palade bodies contain pre-synthesised P-selectin

This enables very rapid (minutes) activation of endothelium (ie binding of leukocytes)

37
Q

what are Adhesion molecules Required for?

A

Leukocyte binding to blood vessels

Leukocyte extravasation from blood vessels

Leukocyte migration (chemotaxis) towards inflamed sites

38
Q

what are The 4 stages of Leukocyte Extravasation and Chemotaxis?

A
  1. Rolling- Leukocyte expresses- Mucin type glycoproteins on neutrophils and sialyl-Lewis-X containing glycoproteins bind to P and E Selectin
  2. Firm adhesion- express Integrins bind to ICAMs
  3. Extravasation (diapedesis) Integrins and PECAM (CD31) binds ICAMs and PECAM (CD31) on endothelial cell
  4. Chemotaxis through tissue- express Chemokine receptors bind to Chemokines
39
Q

summarise local inflammation / chemotaxis

A
  1. Initial responses
    - Tissue macrophages detect microbes, release inflammatory mediators, chemokines, cytokines
    - Complement activation releases chemoattractants C3a and C5a
  2. Vascular effects
    - Macrophages and complement products trigger:
    Increase in vascular diameter / permeability
    increased blood flow
    reduced velocity of blood flow
    accumulation of Igs, complement and other blood proteins in the tissue.
    - Up-regulation of adhesion molecules on endothelial cells
  3. PMN and Monocytes adhere and extravasate
    - Selectins on endothelial cells recognize leukocyte glycoproteins (Lewis X) causing them to roll.
    - ICAM-1 on endothelium interacts with LFA-1 (CD11a/CD18) and CR3 (Mac-1 or CD11b/CD18) so that leukocytes attach firmly to the endothelium, cross the vascular endothelial wall and enter site of infection
  4. Leukocytes migrate up chemotactic gradient
    - CXC chemokines promote migration of neutrophils
    e. g. IL-8
    - CC chemokines promote migration of monocytes
    e. g. MCP-1, MIP-1b, RANTES
    - Complement components C3a C5a attract both
    - Also molecules given off by microbe, e.g. fMet
40
Q

what do fMet peptides do?

A
  • As well as being an important chemotactic stimulus for phagocytes, fMet peptides have anti-leukocyte properties
  • fMLP inhibits killing of Staphylococcus epidermidis in vitro
41
Q

name a Bacterial chemotactic compound

A
  • Mycobacterium tuberculosis Lipoarabinomannan (LAM) is chemotactic for macrophages but not neutrophils- maybe used by MTB to encourage granulomas to enhance bacterial survival / dormancy?
  • LAM also inhibits macrophage phagocytosis
42
Q

how have bacteria evolved mechanisms to block chemotaxis of phagocytes?

A

S. aureus inhibits leukocyte chemotaxis using the CHIPS protein

43
Q

what is CHIPS?

A
  • Chemotaxis-inhibitory protein of S. aureus
  • CHIPS is produced by 80% of S. aureus strains
  • CHIPS has potential as a novel anti-inflammatory drug
44
Q

how does CHIPS work?

A
  • CHIPS blocks chemotaxis receptors on leukocytes (fMet R, also affects C5a receptor, a related 7 transmembrane G-protein linked receptor)
  • inhibits leukocyte recruitment
45
Q

Role of formylated peptides in chemotaxis?

A
  • Bacterial protein synthesis starts with fMet-tRNA

- Staphylococcus aureus formylated peptides cause chemotaxis

Infection And Immunity (16 decks)

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