Acute inflammation brings a range of cell types and inflammatory mediators into the area of damage. They have a number of roles and the interaction of each element is dealt with in more detail within the submenu.
- polymorphonuclear granulocytes: appear early and have key role in removing necrotic cells, foreign material and bacteria
- macrophages: more vital role in wound healing. Phagocytose but also release inflammatory mediators with a significant role in healing.
- eosinophils: active role in certain parasitic infections and hypersensitivity
- mast cells: release mediators acting locally e.g. histamine
- endothelial cells: can produce mediators and migrate during the process of angiogenesis
Chemical inflammatory mediators:
- histamine: promotes increased dilatation and permeability of blood vessels
- kinin system: vasodilators, increased vessel permeability and more prolonged extra-vascular smooth muscle stimulant.
- complement: role dependent on component and diverse. Can act as opsonin for phagocytosis, chemoattractant for neutrophils or can be directly bactericidal.
- plasmin: modulates complement and kinin system as well as digestion of fibrin
- prostaglandins: many roles, PGE1 & PGE2 involved in vasodilatation and increased permeability
- cytokines: involved in leukocyte intercellular signalling