ABSTRACT
Introduction Inflammation is the response of tissues to injury or pathogens. It is an ordered process mediated by the appearance of intercellular adhesion molecules on endothelia and various inflammatory mediators released by tissue cells and leukocytes. At the inflammation lesions, activated T cells, macrophages, monocytes, and mediators produced by these cells such as cytokines, eicosanoids, and reactive oxygen species can be found. Cytokines are proteins of low molecular weight, involved in the regulation of local or systemic immune and inflammatory responses. Upon appropriate stimuli such as bacterial endotoxin (lipopolysaccharide, LPS), a wide variety of cell types produce cytokines. Cytokines have extensive biological roles, functioning either locally or systematically in a way similar to hormones. Among cytokines, tumor necrosis factor (TNF) is involved in inflammation and autoimmune reactions (1). Overproduction of TNF-α mediates severe inflammation, triggers the production of other proinflammatory cytokines, enhances acute phase protein synthesis, induces fever and neutrophilia, causes shock in infection, and apoptosis of cells (2). TNF-α is implicated in the pathobiology of many human diseases, including rheumatoid arthritis, multiple sclerosis, and inflammatory bowel disease (3,4). TNF-α has been considered to be a therapeutic target for many diseases (3). Thus, TNF-α was selected for studying inflammatory responses in this investigation.
