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Role of interleukin-17 in the pathogenesis of Legionella longbeachae infection in vivo

Grant number: 16/24049-7
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Start date: December 01, 2016
End date: November 30, 2017
Field of knowledge:Biological Sciences - Immunology - Cellular Immunology
Principal Investigator:Dario Simões Zamboni
Grantee:Yasmin Junqueira Capobianco
Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
Associated research grant:13/08216-2 - CRID - Center for Research in Inflammatory Diseases, AP.CEPID

Abstract

Legionnaires' Disease or Legionellosis is caused by bacteria of the genus Legionella, which accidentally infect human lung cells, resulting in acute pneumonia. Initial bacterial infection is controlled by innate immunity through the activation of several pattern recognition receptors (PRRs). However, Legionella longbeachae, unlike L. pneumophila, does not have flagellin. Thus, there is no activation of NLRs (nod-like receptors) and the control of the bacteria is impaired. These PRRs are also important for the formation of adaptive immunity, composed of a Th1 response with production of IFN-³, TNF and Interleukin-12 (IL-12). In addition, during L. pneumophila infection, IL-17 induces the production of pro-inflammatory molecules such as IL-6, TNF and IL-1² and neutrophil recruitment. Although the role of IL-17 in the protective adaptive immune response during L. pneumophila infection has been shown, the importance of this cytokine in L. longbeachae infection is unknown. Thus the hypothesis of this study is that IL-17, through its inflammatory functions in mucosal tissues, such as the lung, can trigger tissue damage and pathogenesis during experimental infection by L. longbeachae. (AU)

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