Introduction
This topic covers the cells that appear in acute and in chronic inflammation and what each one does.
Cells in acute inflammation
The appearance of white blood cells (WBC) is the key sign:
- Neutrophils - purulent bacterial inflammation (segmented nuclei).
- Eosinophils - allergic reactions (and parasites).
- Lymphocytes - viruses.
- The predominant cells change with time: neutrophils dominate in the first 24 hours but disappear quickly after this; they respond more rapidly to chemokines than other cells and attach more firmly to adhesion molecules.
- Monocytes take over from neutrophils after about 24 hours as the predominating leukocyte.
- Endothelial cells and platelets help mediate inflammation by producing inflammatory mediators.
Cells in chronic inflammation
Chronic inflammation shows a mononuclear infiltrate - lymphocytes, plasma cells, macrophages (also eosinophils and mast cells). It ends with fibrosis - cicatrisation (healing by formation of scar tissue). Vascular proliferation is found, but the permeability of the walls is unchanged.
- Macrophages (from monocytes) - phagocytosis and liberation of cytokines.
- Immunocompetent cells - B and T lymphocytes, plasma cells.
- Epithelioid cells - modified macrophages: elongated, pale-staining, with abundant cytoplasm. In granulomas they are found together with giant multinucleate cells.
- Giant cells - formed by fusion of epithelioid cells / macrophages, with 20 or more nuclei. The nuclei may be arranged at the periphery like a horseshoe or ring, or clustered at two poles (Langhans giant cells - specific granuloma inflammation, derived from fusion of epithelioid cells), or present centrally (foreign body giant cells - non-specific granuloma inflammation, derived from fusion of macrophages).
- Fibroblasts - attracted by macrophages; create new connective tissue.