| Grant number: | 10/50043-0 |
| Support Opportunities: | Research Projects - Thematic Grants |
| Start date: | June 01, 2010 |
| End date: | July 31, 2015 |
| Field of knowledge: | Biological Sciences - Immunology - Immunochemistry |
| Principal Investigator: | Lourdes Isaac |
| Grantee: | Lourdes Isaac |
| Host Institution: | Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil |
| City of the host institution: | São Paulo |
| Principal investigators | Angela Silva Barbosa |
| Associated scholarship(s): | 11/15733-8 - Role of complement component C5 to in vivo leptospirose control in murine models, BP.MS |
Abstract
Leptospirosis is one of the most important worldwide zoonoses and is caused by Leptospira. These bacteria are spread mostly through the urine from contaminated rodents. The immune response is essential for host protection and the activation of the complement system is important for bacteria killing. The characterization of how pathogens evade complement attack is a developing field of great relevance. Recently, it has been demonstrated that nonpathogenic Leptospira strains are rapidly killed by the complement system, whereas pathogenic strains are able to resist serum bactericidal activity. However, limited knowledge is available concerning the mechanisms employed by these bacteria to circumvent this major line of defense. In order to improve our understanding of the interactions between Leptospira and the host complement system, four main questions will be addressed in this project: 1) Do pathogenic and nonpathogenic leptospiral strains interact differentially with properdin, the positive regulator of the alternative pathway of complement activation? 2) Pathogenic Leptospira strains acquire host's negative complement regulators C4b-Binding Protein and Factor H. What are the bacterial ligands (surface molecules) involved in these interactions? 3) Do pathogenic Leptospira spp. employ other strategies to evade complement attack? Do they produce proteases capable of degrading crucial complement components? 4) Is the complement system capable of controlling infection by Leptospira? To address this particular question, an in vivo murine model will be established. We believe that a better comprehension of these processes will be useful for the development of new therapeutic strategies for the treatment of leptospirosis. (AU)
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