Inflammation is a non-specific response of the microcirculation which follows tissue damage. After injury or lytic infections the local microvasculature dilates. Vessel wall permeability increases and this, coupled with the increased blood flow, leads to localized tissue edema. The chemical mediators of inflammation are diverse, and an individual mediator will usually be responsible for some, but not all, of the signs of inflammation. For example, interleukin 1 (IL-1), derived from macrophages and other sources, has systemic proinflammatory effects, causing the febrile response, hepatic acute phase protein release, and further leukocyte release from the bone marrow. Locally it increases vascular permeability and activates synthesis of matrix-destructive enzymes, thus amplifying inflammation.

The collective effect of all the inflammatory mediators is to generate the cardinal signs of inflammation: heat ( ca/or), swelling (tumor), pain (do/or), redness (rubor), and loss of function (/asae functio) which results from the swelling and pain. Inflammation promotes the induction of an immune response in three ways.

The passage of soluble components of the immune system within blood (particularly antibody and complement) is increased. Both antibody and complement contribute to further release of inflammatory mediators, and hence amplify the ongoing response.

The passage through tissue of the principal effector cells of the immune system, which recirculate between blood and lymphoid tissue, is increased. In inflammation, the endothelium of the postcapillary venule expresses a range of adhesion molecules which allow the attachment of leukocytes and their movement through the vessel wall. Once within the tissues, these cells are further attracted to the site of inflammation by chemotaxis. Receptors on the cells are sensitive to some of the mediators released at the inflammatory site. The cellular infiltrate associated with acute inflammation initially consists principally of phagocytic neutrophils (or eosinophils in regions where helminth infections are common). Monocytes, which are the circulating precursors of macrophages, a principal phagocytic cell of the immune system, arrive at the inflammatory site 12 to 24 h after the onset of inflammation. Monocytes differentiate, activating as a phenotype with macrophage effector mechanisms. Activated macrophages, in turn, are major producers of inflammatory mediators and can play a central role in amplifying ongoing responses to pathological levels. In some cases, the site of infection is also infiltrated by T lymphocytes, which play a key role in macrophage activation.

Migration of 'antigen-presenting' cells out of damaged infected tissues into lymphoid organs is induced. Every tissue contains a population of hemopoetic 'antigen-presenting' cells (sometimes collectively referred to as the dendritic lineage) which function as 'sentries' of the immune system. In response to some local inflammatory mediators (e.g. cytokines IL-1 or tumor necrosis factor-a) these cells activate and migrate to the draining lymphoid tissue via the afferent lymphatics, carrying antigen from the local site. Once at their target tissue, they activate antigen-specific T lymphocytes and hence an antigen-specific response.

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