Inflammation could be defined as the complex biological response of vascular tissue to harmful stimuli such as pathogen, damaged cells or irritants. It is a protective attempt by the organism to remove injurious stimuli as well as initiate the healing process for the tissue. This is achieved by diluting, destroying or otherwise neutralizing harmful agents (e.g. microbes or toxins) with the subsequent activation of events that lead to eventual healing and reconstitution at site of injury. (Mitchell and Cotran 2004). In the absence of inflammation, wounds and infections would never heal and progressive destruction of tissue would compromise the survival of the organism. Inflammation may become aberrant and harmful like other vital process (Ringler 1997). The cardinal signs of inflammation as stated by cells (30BC-38AD) are rubor et tumour cum palore et docore which when translated means redness and swelling with heat and pain. Function laesa(loss of function) was added by Virchow (1985) as the fifth cardinal sign of inflammatory. Redness arise due to great increase blood flow to the inflamed part while the swelling is as a result of increased flow of blood as well as additional presence of substance that have exuded from the blood vessel into the surrounding tissue (exudates). The heat arises from the increased flow of blood carrying warmth to the periphery from higher Interior temperature of the body. The pain results from increased pressure upon nerve endings and irritating effects of the toxic products of injurious agents, loss of function is due to the pain initiated reflex inhibition of muscle movement, mechanical swelling and tissue destruction ( Ihedioha 2003). INFLAMMATORY AND MEDIATORS
1.1.1 Chemical mediators of inflammation
Mediators originate either from plasma or from cells. Plasma derived mediators (e.g) complement protein Kinins) once present in plasma in precursor forms that must be activated, usually by a series photolytic. Clearages, to acquire their biological properties ( dipro et al.2000). Mast cells and basophiles act primarily by releasing 1gE – mediated inflammation. They are especially abundant in the skin, lungs and nasal mucosa. Granules within the mast cell contain large amount of preformed mediators such as histamine, heparin serotonin etc. Mast cells can phargocitized, destroy, and present bacterial antigens to T- lymphocytes. Cell derived mediators are normally sequestered in intracellular granules that need to be secreted (e.g. histamine in mast cell granules) or synthesized de novo (e.g. prostaglandin, cytokines) in response to stimulus. The major cellular sources are platelets, neutrophils, monocytes, macrophages and mast cells by mesenchymal cells endothelium, smooth muscles fibroblast) and most epithelia earn also be induced to elaborate some of the mediators. The production of active mediators in triggered by microbial products or by host proteins, such as the proteins of the complements, kinin, and coagulation system, that are themselves activated by microbes and damaged tissues. Most mediators perform their biologic activity by initially binding to specific receptor on target cells. Some, however, have direct enzymatic activity (e.g. lysosomal proteases) or mediate oxidative damage ( e.g. reactive oxygen and nitrogen intermediates). One mediator can stimulate the release of other mediators by target cells themselves. The secondary mediators may be identical similar to the initial mediators but may also have opposing activities. They provide mechanism for applying or in certain instances counteracting the initial mediator action. -Mediators can act on one or few target cell types, have diverse targets, or may even have differing types of cells. -Once activated and released from the cell, most of these mediators are short-level. They quickly delay...