Inflammation III Flashcards
Inflammation, tissue injury and attempts at repair coexist in
Chronic Inflammation
Causes of chronic inflammation
- Persistent infections
- Hypersensitivity diseases eg rheumatoid arthritis, multiple sclerosis
- Prolonged exposure to potentially toxic agents eg silicosis, atherosclerosis
Microorganisms often evoke an immune reaction called
Delayed-type hypersensitivity
Morphological features of chronic inflammation
- Infiltration with mononuclear cells
- Tissue destruction
- Attempts at healing (accomplished by angiogenesis and fibrosis)
The half-life of blood monocytes is
1 day
Life span of tissue macrophages
Several months or years
Two major pathways of macrophage activation
Classical
Alternative
Dominant cell type in chronic inflammation
macrophages
Classical macrophage activation may be induced by: (4)
- Microbials(e.g endotoxin) using TLRs
- IFN-Y (T-cell derived signal)
- Foreign substances (crystals, foreign matter)
- M1 macrophages (produce NO and ROS, upregulate lysosomal enzymes)
NB: M1 macrophages - Classically activated macrophages
Main function of M1 macrophages
Destroy or Kill microbes
Alternative macrophage activation is induced by
Cytokines other than IFN-Y such as IL-4, IL-13 (produced by T-cells)
The cytokines of the alternative macrophage pathway stimulate/inhibit the classical macrophage pathway
Inhibit
Principal function of M2 macrophages
Tissue repair
M2 macrophages secrete growth factors that
- Promote angiogenesis
- Activate fibroblasts
- Stimulate collagen synthesis
Much of the tissue injury in chronic inflammation is caused by
The products of Activated macrophages
Macrophages secrete mediators of inflammation such as
TNF
IL-1
chemokines
eicosanoids
Macrophages display antigens to and respond to signals from which cells
T lymphocytes
Dominant population in CI seen in autoimmune and other hypersensitivity diseases
Lymphocytes