Lecture 3: Inflammation II Flashcards
3 possible outcomes from acute inflammation
- Regeneration
- Scarring/fibrosis
- Progression to chronic inflammation
Causes of chronic inflammation
- Prolonged injury/irritant exposure
- Immune-mediated disease
- Persistent infection
Cells of chronic inflammation
- Monocytes/macrophages
- Lymphocytes
- Eosinophils
Not PMNs (acute)
T helper subtypes and their cytokines
Th1: pro-inflam. TNF, IL-1, IFNγ
Th2: IL-4, -5, -13
Th17: IL-17, PMN recruitment
Neutrophils vs macrophages (both phagocytes)
PMNs: much shorter life span, respiratory burst, low iNOS levels, prominent degranulation, NETs, lysosomal enzyme release
Chronic inflammation process
Persistent tissue injury -> inflam./T cell/macrophage cytokines -> fibroblast recruitment/differentiation -> scarring/fibrosis
Layers of chronic inflammation wounds
Occurs w/ deeper, more severe wounds
1. Fibrinopurulent exudate (fibrin/PMNs)
2. Granulation tissue (capillary network w/ fibroconnective tissue/ECM)
3. Scarring
TNF
Works in local concentrations; drives chronic inflammation by increasing inflam. cell recruitment and MMP, PG secretion by synovial cells. Inhib. as treatment for many diseases
IL-6
Synthesized by many different cells. Triggers:
- Acute phase reactant synth. by liver
- Systemic fever
- B cell growth
Acute Phase Proteins
Induced by cytokines, synth. in liver. Plasma proteins that are an inflammatory marker e.g. CRP. Measured w/ ESR
Granulomatous inflammation
Assoc. w/ specific pathologic conditions; formation of granuloma in attempt to eliminate/contain insult too large for a single cell
Granuloma
Macrophage + other cells aggregate around large pathogen/irritant (epitheliod macrophages, lymphocytes, fibroblasts, multinucleated giant cells