4.6 Article

Low levels of TNFA gene expression seem to favor the development of pulmonary tuberculosis in a population from the Brazilian Amazon

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IMMUNOBIOLOGY
卷 228, 期 2, 页码 -

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ELSEVIER GMBH
DOI: 10.1016/j.im.2022.103744

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Tuberculosis; TNF-; IL-10; Polymorphism; Gene expression; Amazon

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This study investigated the association of TNFA-308G/A and IL10-819C/T polymorphisms and TNFA and IL10 gene expression levels with pulmonary and extrapulmonary tuberculosis. The study found that TNFA-308G/A polymorphisms were associated with extrapulmonary tuberculosis, but not with pulmonary tuberculosis. The expression levels of TNFA were lower in patients with pulmonary tuberculosis, and there was a positive correlation between TNFA and IL10 expression levels in these patients. This suggests that reduced TNFA expression levels may promote the formation of an anti-inflammatory microenvironment, contributing to the persistence of the bacillus in the host and the establishment of pulmonary tuberculosis.
TNF-alpha is a Th1 cytokine profile active in the control of Mycobacterium tuberculosis infection, IL-10 is associated with persistence of bacterial infection. The aim of the study was to investigate the association of TNFA-308G/A and IL10-819C/T polymorphisms and TNFA and IL10 gene expression levels with pulmonary and extrapulmo-nary tuberculosis (n = 200) and control (n = 200). The individuals were submitted to genotyping and quanti-fication of gene expression performed by real-time quantitative polymerase chain reaction (qPCR). No association was observed between the frequencies of polymorphisms evaluated and pulmonary tuberculosis. The frequency of polymorphic genotypes for TNFA -308G/A were associated with the extrapulmonary tuberculosis (p = 0.0445). The levels of TNFA expression were lower in the pulmonary tuberculosis group than in the control (p = 0.0009). There was a positive correlation between the levels of TNFA and IL10 in patients with pulmonary tuberculosis (r = 0.560; p = 0.0103). Reduced levels of TNFA expression may promote the formation of an anti-inflammatory microenvironment, favoring the persistence of the bacillus in the host, contributing to the establishment of pulmonary tuberculosis.

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