LYCOS RETRIEVER 
Inflammation: Chronic Inflammation
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Many common cancers develop as a consequence of years of chronic inflammation. Increasing evidence indicates that the inflammation may result from persistent mucosal or epithelial cell colonization by microorganisms; including hepatitis B virus and hepatitis C virus, which can cause hepatocellular cancer; human papilloma virus subtypes, which cause cervical cancer, and the bacterium Helicobacter pylori, which can cause gastric cancer. At present, the cause of other chronic inflammatory conditions associated with increased cancer risk, such as ulcerative colitis, is obscure. Particular microbial characteristics as well as the type of the inflammatory response contribute to clinical outcomes via influence on epithelial cell and immune responses. Persistent inflammation leads to increased cellular turnover, especially in the epithelium, and provides selection pressure that result in the emergence of cells that are at high risk for malignant transformation. Cytokines, chemokines, free radicals, and growth factors modulate microbial populations that colonize the host.
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Scientists now believe that chronic inflammation is involved in the development of major depression that precedes Alzheimer’s disease. Chronic inflammatory changes that are suspected to be a common feature of depression could predispose depressed patients to neurodegenerative changes in later life. In support of this theory, clinical evidence shows that depression commonly precedes Alzheimer’s disease and may be an early manifestation of dementia before cognitive decline becomes apparent. Evidence indicates that chronic low-grade inflammation changes brain structure in a way similar to that seen in Alzheimer’s disease and other dementias. Neuronal loss, for example, is a common feature of major depression and dementia. Scientists have hypothesized that the activation of macrophages in the blood and brain release pro-inflammatory cytokines, which encourages the progress from depression to dementia.
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Vasogen is a leader in the research and commercial development of immune modulation therapies targeting the chronic inflammation underlying cardiovascular disorders. Inflammation is a normal response of the immune system to cellular injury caused by infection, trauma, or other stimuli. During the inflammatory process, immune cells are attracted to the site of inflammation where they release cytokines - potent chemical messengers that control inflammation and facilitate the healing process. While inflammation is normally self-limiting, it can persist and become chronic. Recent advances in medical research have established the fundamental role of chronic inflammation in the development and progression of a number of serious conditions, including heart failure, atherosclerosis, and neurodegenerative diseases.
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HMGB1 is expressed at high levels beginning 12 to 72 hours after an injury, which is about the time inflammation-associated tissue damage begins. Because of the timing and duration of expression of HMGB1, it may be an important factor in the sequence of events that result in severe tissue damage following injury or during chronic inflammation. MedImmune's HMGB1 program is being conducted in collaboration with Critical Therapeutics, Inc.
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Few will argue that it is important to control inflammation to reduce disease and enhance health. However, the way in which one controls inflammation is open for debate. The risk of pharmaceutical COX-2 inhibitors has recently been exposed. Vioxx® was recently removed from the market by its maker, Merck, because it caused significant increase in the risk of heart attacks. Soon afterwards, Pfizer announced that Celebrex® raises the risk of adverse cardiovascular events by 250%, and now the safety of Aleve is being questioned. There's no doubt that the long-term use of these drugs for chronic inflammation is very risky.
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The cellular component involves leukocytes, which normally reside in blood and must move into the inflamed tissue via extravasation to aid in inflammation. Some act as phagocytes, ingesting bacteria, viruses, and cellular debris. Others release enzymatic granules which damage pathogenic invaders. Leukocytes ... release inflammatory mediators which develop and maintain the inflammatory response. Generally speaking, acute inflammation is mediated by granulocytes, while chronic inflammation is mediated by mononuclear cells such as monocytes and lymphocytes.
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Chronic Inflammation