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Immunology II > Inflammation I > Flashcards

Inflammation I Flashcards

1
Q

Acute inflammation

A

Minutes - hours
Mainly neutrophils
Usually mild and self limiting
Prominent local and systemic signs

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2
Q

Chronic inflammation

A

Days
Monocytes/macrophages and lymphocytes
Often severe and progressive tissue injury and fibrosis
Less local and systemic signs

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3
Q

Causes of acute inflammation

A

Infections
Tissue necrosis from ischemia, trauma, and physical/chemical injury
Foreign bodies
Immune or hypersensitivity rxns

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4
Q

Mechanism of microbe recognition

A

Cellular receptor for microbes (TLRs)
Cytosol receptors that recognize molecules released with cell damage
Other cellular receptors involved in inflammation
Circulating proteins (complement system)

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5
Q

Signs of inflammation

A

Redness
Swelling
Heat
Pain

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6
Q

Vascular changes in acute inflammation

A

Vasodilation (heat and redness)
Increased permeability of microvasculature, causing edema, an excess of interstitial fluid or cavity fluid
Stasis of blood flow (vascular congestion)
Neutrophils marinate, adhere to endothelium and then migrate through vessel into interstitium

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7
Q

Exudate

A

Fluid high in protein and cellular content

Pus: purulent exudate rich in wbc, necrotic debris, and sometimes microbes

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8
Q

Transudate

A

Fluid low in protein and cellular content

Associated with low serum albumin or increase hydrostatic pressure (such as heart failure)

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9
Q

Cellular events in acute inflammation

A

Extravasation: journey of leukocyte from vessel lumen to interstitial tissue
Steps involved:
1. Adhesion of leukocyte to vascular endothelium
2. Transmigration across endothelium (diapedesis)
3. Chemotaxis
4. Leukocyte activation
5. Phagocytosis

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10
Q

Inflammatory mediators

A

Redistribution of adhesion molecule P-selectin (redistribution induced by histamine and thrombin and activated by cytokines, histamine, or thrombin)
Induction of adhesion molecule synthesis of E-selectin and ligand for integrins (VCAM1, ICAM1) in endothelial cells in 2-3hrs (induced by IL1 and TNF)
Increase in binding affinity of leukocyte integrins induced by chemokines

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11
Q

Transmigration/Diapedesis

A

Migration of leukocytes through endothelium
After transverse game endothelium, leukocytes pierce basement membrane (probably secrete collagenases and enter extravascular tissue)
Neutrophils predominate cells that transmigrate during acute inflammation

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12
Q

Chemotaxis

A

Exogenous: originating from source of inflammation
Bacterial products
Endogenous: produced by injured host
Complement components (C5a), leukotriene B4 (LTB4), and chemokines (IL8)
Chemoattractants induce leukocyte movement -> binds receptor -> activates phospholipase C -> inc intracellular Ca -> triggers cross linking of actin -> pseudopod

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13
Q

Activation of leukocytes

A
  1. Recognition of offending agents which signals

2. Activate leukocytes to ingest and destroy offending agents and amplify inflammatory reaction

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14
Q

Response to leukocyte activation

A
  1. Amplification of inflammatory reaction
    Produce arachidonic acid metabolites by leukocyte
    Secretion of cytokines by leukocyte
  2. Degranulation and release of lysosomal enzymes
  3. Phagocytosis and activation of oxidative burst within leukocyte
  4. Increase in binding affinity of adhesion molecules
  5. Chemotaxis
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15
Q

Nitric oxide

A

Soluble gas produced by endothelial cells and macrophages
Vasodilator
Kills microorganisms

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16
Q

Neutrophil extracellular traps (NETS)

A

Fibrillary networks containing antimicrobial substances produced by neutrophils
Microbes caught in fibrils
Consists of:
1. Nuclear chromatin (neutrophil extrudes it nucleus killing the cell)
2. Contents of cytoplasmic granules which contain antimicrobial proteins and enzymes

17
Q

Major inflammatory mediators

A

Vasoactive amines
Lipid products (prostaglandins and leukotrienes)
Cytokines, including chemokines
Complement

One mediator can stimulate release of other mediators

18
Q

Vasoactive amines

A

Histamine: mast cells, basophils, platelets
Dilation of arterioles and increase permeability of venules by producing interendothelial gaps due to contraction of endothelial cells
Induce synthesis of prostacyclin and nitric oxide
Serotonin: platelets and some neuroendocrine cells
Released with histamine during platelet aggregation
Vasoconstrictor
Neurotransmitter in GI tract

19
Q

Arachidonic acid metabolites

A

Concerted by enzymes into prostaglandins and leukotrienes when cells are activated by diverse stimuli

20
Q

Cyclooxygenase pathway products

A

PGI2 (prostacyclin): vasodilation and inhibits platelet aggregation
Thromboxane A2: vasoconstriction and promotes platelet aggregation
PGD2, PGE2, and PGF2: vasodilation, potentiate edema by enhancing vascular permeability effects of other mediators (PGE2 pain and involved in cytokine, induced fever with infections)

21
Q

Lipoxygenase pathway products

A

Leukotrienes B4: neutrophil chemotaxis
Leukotriene C4, D4, and E4: increase vascular permeability by endothelial cell contraction, vasoconstriction, bronchospasm
Lipoxins A4 and B4: INHIBITOR of inflammation

22
Q

Cytokines and chemokines

A

Cytokines: mediate and regulate immune and inflammatory rxns
IL1 and TNF
Chemokines: small proteins acting as chemoattractants

23
Q

Complement system

A 
Enzymatic cascade
C5b-C9: membrane attack complex
C3a, C5a: anaphylatoxins, stimulate release of histamine
C5a: leukocyte chemotactic factor
C3b: opsonin
24
Q

Regulatory proteins of complement

A

C1 inhibitor: block activation of C1
Decay accelerating factor (DAF): prevents formation of C3 convertase
CD59: inhibits formation of membrane attack complex

25
Q

Platelet Activating Factor

A

Causes platelet aggregation
Vasoconstriction and bronchoconstriction
Increased leukocyte adhesion to endothelium, chemotaxis, degranulation, and oxidative burst
Boosts synthesis of other mediators, especially eicosanoids

26
Q

Kinin system

A

Vasoactive peptides
Kallikrein cleaves kininogen into bradykinin
Bradykinin: vasodilation and increased vascular permeability, major contributor to pain, bronchoconstriction

Immunology II (9 decks)

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