Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8962277 | Tuberculosis | 2018 | 26 Pages |
Abstract
Given the impossibility to study the lung immune response during Mycobacterium tuberculosis-latent infection, and consequently, the mechanisms that control the bacterial load, it is reasonable to determine the activation of local immunity in the early phase of the infection. The phosphatidylinositol-3-kinase gamma enzyme (PI3Kγ) is involved in the leukocyte recruitment, phagocytosis and cellular differentiation, and therefore, it is considered a promising target for the development of immunotherapies for chronic inflammatory diseases. Mice genetically deficient in PI3Kγ (PI3Kγâ/-) or WT (Wild Type) were evaluated 15 days post-infection. The enzyme deficiency improved the resistance against infection, increased the frequency of CD4+IL-17+ cells, the production of IL-17 as well as the gene and protein expression of molecules associated with Th17â¯cell differentiation and neutrophil recruitment. Our findings show, for the first time, the participation of the PI3Kγ in vivo in the M. tuberculosis-infection, and suggest an association of Th17â¯cells with protection in the early phase of tuberculosis.
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Authors
M.P. Cavalcanti-Neto, R.Q. Prado, A.R. Piñeros, C.A. Sérgio, T.B. Bertolini, A.F. Gembre, S.G. Ramos, V.L. Bonato,