Inflammation & Wound Healing Flashcards by McKinzie Neggers

acute inflammation is characterized by

edema and neutrophils (innate immunity)

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Toll-like receptors

on innate and adaptive immune cells

activated by pathogen-associated molecular patterns (PAMPs) –> upregulated NF-kB

ie CD14 — LPS

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arachidonic acid is released by

phospholipase A2

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cyclooxygenase produces

prostaglandins

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5-lipoxygenase produces

leukotrienes

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prostaglandins mediate

PGI2, PGD2, PGE2 mediate vasodilation of arterioles and post-capillary vascular permeability

PGE2 mediates fever

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leukotrienes mediate

LTC4, LTD4, LTE4 cause vasoconstriction, bronchospasm, and increase vascular permeability

ie smooth muscle contraction

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what attracts and activates neutrophils?

LTB4
C5a
IL-8
bacterial products

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mast cells are activated by

tissue trauma
C3a, C5a
crossing linking by IgE antigen

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classical pathway activation

C1 bings IgG or IgM bound to antigen

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alternate pathway activation

microbial products directly activate complement

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mannose-binding lectin pathway

MBL binds to mannose of microbes

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mast cells immediately

release histamine

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mast cells delayed response

produce leukotrienes

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Hageman factor (factor XII) activates

1) coagulation and fibrinolytic systems
2) complement
3) kinin system (HMWK –> bradykinin)

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redness and warmth due to

vasodilation

key mediators: histamine, prostaglandins, bradykinin

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swelling due to

leakage of fluid from postcap venules

key mediators: histamine, tissue damage

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pain due to

sensitized nerve endings

key mediators: bradykinin and PGE2

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fever due to

pyrogens cause macrophages to release IL-1 and TNF –> increased cyclooxygenase activity in perivascular cells in hypothalamus

key mediators: PGE2

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margination involves

vasodilation and cells flowing to the periphery

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rolling involves

selectin on endothelial cells binding to sialyl Lewis X on leukocytes

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P-selectin is released from

Weibel-Palade bodies, mediated by histamine

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E-selectin is induced by

TNF and IL-1

adhesion

interaction of CAMs and integrins

integrins are upregulated by

C5a and LTB4

CAMs are upregulated by

TNF and IL-1

leukocyte adhesion deficiency

CD18 on integrins clinically see delayed separation of umbilical cord, increased circulating neutrophils, increased bac infection w/ no pus

neutrophils are attracted by

IL-8, C5a, LTB4

phagocytosis is enhanced by

IgG and C3b

Chediak-Higashi syndrome has

impaired phagolysosome formation clinically: pyogenic infection, neutropenia, giant granules in leukocytes, defective primary hemostasis, albinism, peripheral neuropathy

killing in phagolysosomes done by

HOCl O2 --> O2- --> H2O2 --> HOCl enzymes: NADPH oxidase, SOD, MPO

Chronic granulomatous disease is characterized by

poor O2 dependent killing due to NADPH oxidase defect clinically: infection with catalase (+) organisms test with NBT dye: colorless = (+)

MPO deficiency is characterized by

increased risk of Candida infections

macrophage peak at

2-3 days after inflammation begins | kill via lysozymes

anti-infammatory cytokines produced by macrophages

IL-10 and TGF-B = resolution and healing

produced by macrophages to recruit more neutrophils

IL-8 = continued acute inflammation

abscess is

acute inflammation surrounded by fibrosis

macrophages produce chronic inflammation when

macrophages present antigen to CD4+ helper T cells

chronic inflammation characterized by

presence of lymphocytes and plasma cells

CD4 helper T cell activation

1. MHC class II (antigen presenting cell) ---- TCR complex (CD4 T-cell) 2. B7 (antigen presenting cell) ---- CD28 (CD4 T-cell)

T-cell receptor complex is

TCR + CD3

activated CD4 secrete

cytokines Th1 and Th2

Th1 secretes

IFN-y which activates macrophages, IgM class switching from IgM to IgG, inhibits Th2

Th2 secretes

IL-4 which promotes B-cell class switching to IgE, IL-5 causes eosinophil chemotaxis and switching to IgA, IL-13 which is similar to IL-4

IL-4 promotes

B-cell class switching to IgE

IL-5 causes

eosinophil chemotaxis and B-cell class switching to IgA

IL-13 is similar to

IL-4

CD8 cytotoxic T-cell activation

1. MHC class I (on all nucleated cells) ----- TCR complex (CD8 T-cell) 2. IL-2 (CD4 Th1 cell)

CD8 cytotoxic T-cells induce apoptosis by

1. secretion of perforin and granzyme | 2. expression FasL

B-cell activation occurs via

either: 1. antigen binding to surface IgM or IgD or 2. MHC class II (B-cell) ----- TCR complex (CD4) and CD 40 (B-cell) ----- CD40L (CD4 T-cell)

key cell of a granuloma is

epithelioid histiocytes (macrophages w abundant pink cytoplasm)

granuloma is surrounded by

giant cells and rim of lymphocytes

noncaseating granulomas

lack central necrosis ie sarcoidosis, beryllium exposure, Crohn dz, cat scratch dz

caseating granulomas have

central necrosis ie TB, fungal infection

macrophages secrete IL-12 which induces

CD4 helper T cells to differentiate into Th1 subtype

IFN-y helps convert macrophages into

epithelioid histiocytes and giant cells