[Th1 immune response induced by Mycobacterium tuberculosis H37Ra in NOD2 knockout mice].

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi

School of Basic Medicine, Ningxia Medical University, Ningxia Key laboratory of Clinical and Pathogenic Microbiology, General Hospital of Ningxia Medical University, Yinchuan 750004, China. *Corresponding author, E-mail:

Published: July 2019

Objective To investigate the roles of Th1 cytokines tumor necrosis factor α (TNF-α), interferon gamma (IFN-γ) and multifunctional T cells in nucleotides binding oligomer domain 2 knockout (NOD2) mice infected with Mycobacterium tuberculosis (MTB) H37Ra. Methods Mouse models of pulmonary infection were established by tracheal instillation of MTB strain H37Ra into NOD2 mice and C57BL/6 mice (n=10 each group). Lung tissues were removed and stained by HE staining and pathological scores were evaluated 4 weeks after infection. The levels of TNF-α and IFN-γ in the lung homogenates were detected by ELISA, and the ratio of multifunctional CD4 T and CD8 T cells in the spleen were examined by flow cytometry. Results MTB infection promoted lung inflammation of NOD2 mice. The levels of TNF-α and IFN-γ in the lung tissues of NOD2 mice increased. Compared with normal saline group, TNF-α, IFN-γ cells and TNF-αIFN-γ cells in CD4/CD8T cells significantly increased in NOD2 mice and C57BL/6 mice after the infection. TNF-αCD4T cells, IFN-γCD4T cells and IFN-γCD8T cells in MTB-infected NOD2 mice were significantly higher than those in MTB-infected C57BL/6 mice. Conclusion H37Ra can induce Th1 immune response in NOD2 mice.

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