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CIGARETTE SMOKE EFFECTS IN INFLAMMATORY RESPONSE OF THE CENTRAL NERVOUS SYSTEM

Grant number: 11/15435-7
Support type:Scholarships in Brazil - Master
Effective date (Start): March 01, 2012
Effective date (End): February 28, 2014
Field of knowledge:Health Sciences - Pharmacy - Toxicological Analysis
Principal researcher:Tania Marcourakis
Grantee:Ana Carolina Cardoso dos Santos Durão
Home Institution: Faculdade de Ciências Farmacêuticas (FCF). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

Smoking is a major cause of chronic diseases leading to exacerbate hypertension, coronary heart diseases and others. It is expected that 1.6 billion people will become smokers in 2030. In 1999, these data led to the creation of tobacco control politics to prevent contamination of nonsmokers by environmental pollution caused by smoking, once smoke is associated with allergic reactions, acute myocardial infarction, lung cancer and chronic obstructive pulmonary diseases. The innate immune system is responsible for the quick and nonspecific inflammatory response against tissue injuries, bacteria and viruses. The main form of antigen presentation on the innate immune system is by PPRs (antigen recognition receptors) which can recognize PAMPs (patterns associated antigen, triggering a cascade of reactions that culminate in the activation of immune response. The lipopolysaccharide (LPS), PAMP of Gram-negative bacteria, is recognized by the TLR4 (toll-like receptor). This connection is effective when LPS is shielded by a protein called LBP that, once the complex LPS-LBP is formed, it binds to a glicosilphosphatidilinositol - CD14 - and then connect to TLR4-MD2 dimmer. This connection triggers a response that is My88-dependent and lead to the activation of the nuclear factor ºB (NF-ºB), responsible for the transcription activation of pro- and antiinflammatory cytokines such as IL6 and IL10, which are important to the inflammatory process. There are evidences describing the inflammatory action of cigarette smoke in lungs and in bone marrow cells, however, little is known about its effects on central nervous system (CNS). Previous studies from our research group have showed that cigarette smoke induces changes in antioxidant enzymes as well as lipid peroxidation in the CNS of mice. This study aims to clarify whether exposure to cigarette smoke for 15 consecutive days induces neuroinflammatory in B57/BL6 mice. To do so, pro- and anti-inflammatory cytokines (IL6, IL1², IL10, TNF), membrane receptors TLR2 and TLR4, iNOS and NF-ºB will be evaluated.

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