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Investigation upon a role of neutrophils and their COX-2 expression on hyperalgesy development during experimental colitis

Grant number: 14/05649-8
Support type:Scholarships in Brazil - Post-Doctorate
Effective date (Start): July 01, 2014
Effective date (End): July 01, 2017
Field of knowledge:Biological Sciences - Physiology
Principal Investigator:Carlos Amilcar Parada
Grantee:Felipe Meira de Faria
Home Institution: Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil
Associated scholarship(s):14/14634-4 - The contribution of neutrophil COX-2 expression to inflammatory bowel disease, BE.EP.PD

Abstract

Despite the unknown origin, the knowledge on the pathogenesis of IBD has grown dramatically over the last years and most of such advance is due the use of experimental animal models of IBD. Over the last years, many researches using transgenic animals and chemical induced models have shown to be very informative regarding the mechanisms involved in development and repair of intestinal inflammation. For that, it is important to not only explore the peripheral mediators of inflammation but also the drivers of the immune-inflammatory response, however neuro-immune modulation may be the platform that serves to interface the disease experience and the these mediators. The immune system can influence nervous system activity through the release of inflammatory mediators and cytokines. In turn, the nervous system, including the brain and peripheral neurons, can stimulate or inhibit activities of the innate and adaptive immune response, by acting on inflammatory cells. Considering the recent advances upon interaction between gastrointestinal tract and nervous system on pain during colitis, very little is known upon the contribution of inflammatory cells on the development of hyperalgesia during colitis. It's known that as part of the normal gut inflammatory response, neutrophils are recruited to sites of infection or inflammatory stimuli within minute. Despite the beneficial effects of neutrophils for mucosal homeostasis, it is clear that neutrophils also directly contribute to disease pathology; their excessive recruitment and activation leads to release of toxic products and massive trans-epithelial migration, resulting in crypt abscesses and extensive mucosal injury. Thus, the overall profile of eicosanoids generated by neutrophils may clearly influence the way these cells participate in orchestrating the inflammatory response and, as such, a better understanding of the mechanisms controlling their biosynthesis is of fundamental interest for colitis and hyperalgesy. In this context, neutrophils seem to have an important role on inflammatory response during colitis. Based on aforementioned, we are suggesting that neutrophils can have an important role on hyperalgesy development during colitis.