Difference between revisions of "Inflammation mechanism"

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Latest revision as of 10:25, 2 August 2015

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Inflammation mechanism

Recent scientific studies have advanced the notion of chronic inflammation as a major risk factor underlying aging and age-related diseases. Both acute and chronic inflammations are physiological protective mechanisms that act in response to cellular injury or tissue destruction. Inflammatory reactions are known to be extremely complex, but essentially are a well-orchestrated series of physiological cellular reactionary events designed to limit insult and promote repair. The actions of many cell types that regulate the inflammatory response depend on reactive oxygen species (ROS) and reactive nitrogen species (RNS). Most of these species are generated as a result of normal metabolism, e.g., NO is synthesized from the amino acid L-arginine by vascular endothelial cells, phagocytes, and many surveillance cell types.

Unresolved inflammation or phagocyte-derived oxidative stress seems to be a prerequisite or a common thread in meditation of the genesis of a wide range of age-associated neurodegenerative or autoimmune diseases, including atherosclerosis, osteoarthritis, rheumatoid and psoriasis arthritis, multiple sclerosis, lupus, fibromyalgia, Parkinson’s, stroke, Alzheimer’s, or mental illnesses (depression), hypertension, asthma, emphysema, ocular allergies, adult on-set diabetes and cardiovascular complications, vasculitis, colitis, gastritis, pancreatitis, nephritis, hepatitis as well as induction of hyperplasia, neoplasia, cancer metastasis, and angiogenesis. For example, numerous markers of inflammation have been reported in the Alzheimer's disease brain, an anti-aging disorder. Inflammation is not simply a response to already existing Alzheimer's pathology, but ultimately becomes a significant source of pathology. The pathogenic potential of inflammation in Alzheimer's disease follows from the inherent destructiveness of inflammatory mechanisms, the postmitotic status of neurons, and the unique interactions of inflammatory markers and cells with pathologic hallmarks of Alzheimer's such as amyloid beta-peptide. That is one of the mechanisms of aging by inflammation.

Two aging-intervention paradigms, namely calorie restriction (CR) and physical exercise, are discussed to substantiate the importance of the suppression of inflammatory process to deter age-related chronic diseases. The anti-oxidative action of CR is best known for its ability to maintain redox balance and suppress the activation of various redox-sensitive, pro-inflammatory transcription factors and signaling pathways. Accumulating evidence indicates that anti-oxidative CR significantly attenuates nuclear factor-kB (NF-kB), tumor necrosis factors (TNF-a and TNFb), interleukins (IL-1b, IL-2, and IL-6), chemokines (IL-8 and RANTES), adhesion molecules (AMs). Furthermore, CR modulates enzymes, such as inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2), both of which are pro-inflammatory and known to increase with age. Another well-known anti-aging intervention, physical exercise, has also emerged as an effective anti-inflammatory intervention. Exercise is also known to increase overall anti-oxidant defense systems including superoxide dismutase (SOD), catalase, and glutathione (GSH) peroxidase.