|Support type:||Scholarships in Brazil - Doctorate|
|Effective date (Start):||March 01, 2009|
|Effective date (End):||February 28, 2013|
|Field of knowledge:||Biological Sciences - Pharmacology - General Pharmacology|
|Principal Investigator:||Edson Antunes|
|Grantee:||Dalize Maria Squebola Cola|
|Home Institution:||Faculdade de Ciências Médicas (FCM). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil|
Eosinophils are inflammatory cells finds in the airways of asthmatics patients and they probably contribute for asthma pathogenesis. The asthma is an airways pathological condition characterized by chronic inflammatory response due to release of inflammatory mediators, deriving from cells with alveolar macrophages, neutrophils, mast cells, lymphocytes and eosinophils. Research in asthmatics patients and experimentation animal shows that eosinophils are the central effector cell responsible for ongoing airway inflammation. Some factors may be implicated in exacerbation of asthma, such as virus and bacterium (Chlamydia sp; Mycoplasma sp; Sthaphylococcus aureus). Sthaphylococcus aureus is a gram-positive bacterium often found and the normal microflora of skin, upper respiratory and gastrointestinal tracts in humans. This bacterium produces and secrets the so-called staphylococcal enterotoxins which are a family of structurally related heat-stable 23 to 24-kDa proteins. Clinical evidences suggest a link between bacterial organism and pathogenesis and/or exacerbation of human airway disease. In addition, several studies report IgE- independent bronchial asthma can be provoked by bacterial infections, including Gram-positive bacteria. Recently, airways exposition to staphylococcal enterotoxin type A and B (SEA and SEB) in rats has been shows to evoke a large influx of neutrophils in brochoalveolar lavage fluid by mechanisms involving complex interactions of different signaling pathways including overexpression of cytokine-induced neutrophil chemoattractant (CIN-2), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), as well as enhanced production of tumor necrosis factor-± (TNF ±) and interleukin-6 (IL-6). Thus, we initiate to years ago, a research project aiming at the clarification of the involved mechanisms in the exacerbation of the allergic pulmonary response (for eosinophils infiltrated in bronchoalveolar lavage (BAL)) in rats airway exposure to staphylococcal enterotoxin. Until this moment, have been showed that rats airway exposure to staphylococcal enterotoxin and ovalbumin challenge, showed an exacerbation eosinophils influx in the brochoalveolar lavage after 24 h antigenic challenge. Recently, in mice; witch this animal species allows to greater experimental possibilities for the agreement of interaction SEA and allergic challenge; we observed increase of the eosinophils influx in the bronchoalveolar lavage after challenge with OVA as well as rats. The experimental strategy of exposition the staphylococcal enterotoxin and challenge with OVA seems to mimic clinical conditions of exacerbation of bronchial asthma, therefore function as a good model to explore in bigger details the nature of this interaction.