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22 Cards in this Set
- Front
- Back
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What are the prototypes for granulomatous inflammation?
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foreign body giant cell & tuberculosis
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* What is a cluster or aggregate of activated macrophages; frequently fused into multinucleated giant cells
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Granuloma
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What type of response does myobacterium TB produce?
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granulomatous inflammation
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in what cell do myobacteria "start" their invasion?
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resident macrophages, by first binding mannose receptor
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how do myobacteria "thrive" in resident macrophages early on?
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"endosomal manipulation" . replication within phagosomes
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How are myobacteria eventually killed in TB?
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Infected macrophages recruit T Cells --> Th1 release cytokines to activate macrophage --> **NO and O2-** help kill myobacteria
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how do granulomas heal?
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fibrosis and may become calcified
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Do granulomas occur from foreign or endogenous materials?
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can be from both. (sutures, TB ... things that are poorly degrading and persistent)
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What factors can increase the chance of reactivation or reinfection from a granuloma (TB)?
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HIV, advanced age, *anti-TNF therapies, *corticosteroids (supress inflammatory and immune rxns)
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In chronic inflammation, what do M2's release and what is the result?
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TGF-B --> stimulate fibrosis
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What are dense infiltration of tissues with lymphocytes, plasma (b-cells) and macrophages a hallmark of?
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chronic inflammation
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What is meant by the reciprocal interaction between lymphocytes and macrophages in chronic inflammation? what mediators are involved?
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lymphocytes (T cells) secrete INFy --> activates macrophages --> which secrete IL-12 --> further stimulating lymphocytes
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Describe the two "types" of macrophages and how each formed:
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1. Classically activated (M1): by microbial products and cytokines
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What condition, involving obstruction by gallstones, bacterial infection, is this and what "category"?
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chronic cholecystitis; chronic inflammation
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What is the etiology of chronic inflammation?
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repeated episodes or persistence of acute inflammation
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What is chronic inflammation accompanied by?
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fibrosis, tissue destruction, and chronic inflammation
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What type of cells induce (extrinsic) apoptosis in hepatocytes (w/ Hep B)? how?
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CTL (CD8 cells);
1. Fas ligand (on CD8) receptor --> death receptor (Fas) on hepatocyte 2. perforins and granzymes |
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What are the five mechanisms of membrane damage?
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1. free radical peroxidation
2. phospholipase activation --> detergent effect 3. MAC --> osmotic lysis 4. bacterial toxins --> direct lysis 5. perforrins by CTLs --> granzymes trigger apoptosis |
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What are the mediators involved in systemic effects of inflammation?
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LPS --> TNFa --> IL-1 --> IL-6 --> CSF (colony stimulating factors: from bone marrow --> leukocytes); NO lowers bp
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What triggers fever?
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pyrogens:
LPS, IL-1, TNFa **target hypothalamus in pathway --> PGE & sympathetic stimulation |
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What else accompanies the systemic effects of inflammation?
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Liver releases "acute phase reactive proteins": e.g. C-reactive protein and mannose binding lectin --> opsonization
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What is the "order" of cytokine release in fever?
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LPS --> TNFa --> IL-1 --> IL-6
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