The Contribution of Inflammatory Cells to the Pathogenesis of Asthma

Inflammation is the response of vascularised tissue to injury and serves to resolve and repair the effect of damage. The factors that initiate inflammation, like those of cell injury, are diverse and include infectious agents (bacteria, viruses and parasites), physical agents (burns, radiation and trauma), chemical agents (drugs, toxins and industrial agents), ischaemic injury to tissues and immunological reactions such as allergy and autoimmunity. The histopathological features of inflammation consist of changes in blood flow and calibre of small blood vessels followed by alterations in vascular permeability and accompanied by a series of changes involving white blood cells. Acute inflammation is of short duration and characterised by exudation of fluid and plasma proteins (oedema) and leucocyte emigration, with granulocytes being prominent. In contrast, chronic inflammation is of longer duration again generally with granulocyte emigration but also with a dense infiltration of lymphocytes and monocytes/macrophages together with proliferation of blood vessels and connective tissue. In certain specialised circumstances, such as allergy and asthma, eosinophils are often found in particularly large numbers. Both acute and chronic inflammation are associated with some degree of fibrin deposition leading to platelet adherence and the release of platelet products. Basophils are also inflammatory cells and are prominent in certain forms of delayed-type hypersensitivity.