Description

Inflammation has been described as the basis of many pathologies of human disease. When one considers the updated signs of inflammation, they would be vasodilation, cell migration, and, in the case of chronic inflammation, cell proliferation, often with an underlying autoimmune basis. Generally, inflammation may be divided into acute, chronic, and autoimmune, although the editors believe that most, if not all, chronic states are often the result of an autoimmune response to an endogenous antigen. Thus, a proper understanding of the inflammatory basis may provide clues to new therapeutic targets not only in classical inflammatory diseases, but atherosclerosis, cancer, and ischemic heart disease as well. The lack of advances in classical inflammatory diseases, such as rheumatoid arthritis, may in part arise from a failure to classify the disease into different forms. That different forms exist is exemplified in patients with differing responses to existing anti-inflammatory drugs, ranging from non-responders to very positive responders for a particular nonsteroidal anti-inflammatory drug (NSAID). Though researchers have progressively unr eled the mechanisms, the story is far from complete. It should also be noted that the inflammatory response is part of the innate immune response, or to use John Hunter’s words in 1795, “inflammation is a salutary response.”  That may be applied in particular to the defensive response to invading micro-organisms.