AUTHOR=Chen Ming , Deng Huan , Zhao Yue , Miao Xueqing , Gu Haiyan , Bi Ying , Zhu Yifan , Guo Yun , Shi Shuang , Xu Jiejing , Zhao Deyu , Liu Feng 

TITLE=Toll-Like Receptor 2 Modulates Pulmonary Inflammation and TNF-α Release Mediated by Mycoplasma pneumoniae

JOURNAL=Frontiers in Cellular and Infection Microbiology

VOLUME=Volume 12 - 2022

YEAR=2022

URL=https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2022.824027

DOI=10.3389/fcimb.2022.824027

ISSN=2235-2988

ABSTRACT=Objectives: To investigate the roles that Toll-like receptors (TLRs) play in lung inflammation mediated by M. pneumoniae.

Methods: The changes in TLRs and TNF-α in peripheral blood of children with MPP were monitored, and the interactions of signaling molecules regulating TNF-α release in A549 cells and neutrophils after M. pneumoniae stimulation were investigated. In TLR2 knockout (TLR2-/-) mice, the levels of TNF-α in bronchial alveolar lavage fluid (BALF) and peripheral blood after mycoplasma infection and the pathological changes in the lung tissue of mice were detected.
Results: TNF-α levels in peripheral blood of children with MPP were higher than those in non-infected children, and children with refractory MPP had the highest levels of TNF-α and TLR2. TNF-α secretion and TLR2, MyD88 and p-p65 levels were increased in stimulated cells. TNF-α secretion was suppressed upon siRNA-mediated TLR2 silencing. Pharmacological inhibition of NF-κB and MyD88 effectively reduced TNF-α expression. Compared with wild-type mice, the TNF-α in serum and BALF decreased, and lung pro-inflammatory response was partially suppressed in TLR2-/- mice.

Conclusion: We concluded that TLR2 regulates M. pneumoniae-mediated lung inflammation and TNF-α release through the TLR2-MyD88-NF-κB signaling pathway.