Role of acetate on experimental allergic asthma: Short fatty acid chain productiong probiotic bacteria as a mechanism of action.

• Grant number: 13/06265-6
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: July 01, 2013
• End date: June 30, 2014
• Field of knowledge: Biological Sciences - Physiology - General Physiology
• Principal Investigator: Caroline Marcantonio Ferreira
• Grantee: Eduardo Mendes
• Host Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil
• Associated research grant: 12/50410-8 - Effects of short-chain fatty acids produced by probiotic bacteria in the prophylaxis and treatment of allergic airway inflammation, AP.JP

Abstract

Role of acetate on experimental allergic asthma: Short fatty acid chain producting probiotic bacteria as a mechanism of action. Asthma affects around 300 million people worldwide, being the fourth leading cause of hospitalization in Brazil. This is a complex respiratory disease that depends on genetic and environmental factors. There are many environmental factors that affect asthma, such as: diet, urbanization and exacerbated use of antibiotics. All these environmental factors could modify intestinal microflora composition. Interestingly, studies indicate that intestinal microflora have an important role in regulating the inflammatory response of asthma. Preliminary data from this study indicate that oral administration of B. longum, a probiotic bacteria which produces acetate, dcreases Th2 inflammation of the airways. One possible mechanism by which bacteria B. longum down regulate Th2 inflammation could be acetate, which has anti-inflammatory effect in some inflammatory diseases, such as colitis. However, the effects of acetate administration on Th2 mediated inflammation has not been fully elucidated. Therefore, the aim of this study is to evaluate the effects of acetate in asthmatic mice. Also, understand if acetate could be a mechanism by which B. longum down regulates airway inflammation.