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Jakarta, 28 Apr 2009
Acute and Chronic Inflammation as a Key Process to Mucosal Injury - Part 4
Chronic Inflammation
In contrast to acute inflammation, which is distinguished by vascular changes, edema, and a largely neutrophilic infiltrate, chronic inflammation is characterized by (i) infiltration with mononuclear cells, including macrophages, lymphocytes, and plasma cells; (ii) tissue destruction, largely induced by the inflammatory cells; and (iii) repair involving new vessel proliferation and fibrosis. Chronic inflammation may follow acute inflammation.
Macrophages are but one component of the mononuclear phagocytes system, including the circulating blood monocytes, and tissue macrophages. The half-life time of circulating monocytes is about 1 day; under the influence of adhesion molecules and chemotactic factors, they begin to emigrate at a site of injury within the first 24-48 hours after onset of acute inflammation. When monocytes reach the extra vascular tissue, they undergo transformation into macrophages, which may become activated. Activation signals includes cytokines secreted by sensitized T lymphocytes, bacterial endotoxins, various mediators produced during acute inflammation. After activation, macrophages secrete a variety of biologically active products such as acid and neutral protease, complement components, reactive oxygen species, NO, eicosanoids, and cytokines.
Other types of cells present in chronic inflammation are lymphocytes, plasma cells, and eosinophils. Both T and B lymphocytes migrate into inflammatory sites via adhesion molecules and chemokines used to recruit monocytes. Plasma cells are the terminally differentiated end-product of B cell activation; they can produce antibodies directed against antigens in the inflammatory site. Eosinophils are characteristically found in inflammatory sites around parasitic infections, or as part of immune reactions mediated by IgE, typically associated with allergies.
Mucosta is an anti gastritis and gastropathy drug with Rebamipide as it’s active ingredient. The molecular weight of Rebamipide is 370.79. Mucosta is classified as anti-inflammatory, anti free-radical drug. As anti-inflammation drug, Mucosta suppress inflammation process due to the release of inflammatory cytokine, such as IL-8, TNF-α, IL-1ß. By inhibiting the release of free radical, superoxide (O2-) and also scavenge hydroxyl radical (OH-) Mucosta shows its action as anti free-radical. Mucosta promotes the synthesis of endogen prostagladin which helps to improve gastroduodenal mucosal defense against aggressive factor, like gastric acid, infection due to H. pylori, NSAIDs, and other stressors.
Mucosta is indicated in treatment of gastritis, gastropathy (due to NSAIDs, steroid, or antibiotics), gastric ulcer, and to prevent acute gastroduodenal mucosal lessions due to administration of NSAIDs, steroid, or antibiotics. Mucosta has strong penetration into gastrointestinal mucosal with minimal systemic effect. Mucosta does not interact and does not interfere with absorption of other drugs which often given together (NSAIDs, antibiotics) . In that way, Mucosta does not affect the effectiveness of those drugs.
References
- Sobala GM., et al. Acute Helycobacter pylori infection : Clinical features, local and systemic immune response, gastric-mucosal histology, and gastric juice ascorbic acid concentrations. Gut 1991; 32: 1415-18.
- Marshall B., et al. Attempt to fulfill Koch’s postulate for pyloric Campylobacter. Med. J. Aust. 1985; 152: 436-9.
- Baggiolini M., et al. Interleukin-8 and related chemotactic cytokines-CXC and CC chemokines. Adv. Immunol. 1994; 55: 97-179.
- Crabtree JE., et al. Mucosal interleukin-8 and Helicobacter pylori associated gastroduodenal disease. Eur. J. Gastroenterol. Hepatol. 1994; 6 (Suppl. 1): S33-S38.
- Crabtree JE., et al. Gastric IL-8 and IL-8 IgA autoantibodies in Helicobacted pylori infection. Scan. J. Immunol. 1993; 37: 65-70.
Philip Darmawan, MD., MKT.
Medical Advisor
pdsony@ho.otsuka.co.id
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