TLR2 regulates Moraxella catarrhalis adhesion to and invasion into alveolar epithelial cells and mediates inflammatory responses

ABSTRACT

Moraxella catarrhalis is a major cause of chronic obstructive pulmonary disease. Toll-like receptor 2 (TLR2) plays an important role in the inflammatory response in host respiratory epithelial cells. M. catarrhalis induces an inflammatory immune response in respiratory epithelial cells that is mostly dependent on TLR2. However, the mechanisms by which this pathogen adheres to and invades the respiratory epithelium are not well understood. The present study aimed to reveal the role of TLR2 in M. catarrhalis adhesion to and invasion into alveolar epithelial cells, using molecular techniques. Pretreatment with the TLR2 inhibitor TLR2-IN-C29 enhanced M. catarrhalis adhesion to A549 cells but reduced its invasion, whereas the agonist Pam3CSK4 reduced both M. catarrhalis adhesion and invasion into A549 cells. Similarly, M. catarrhalis 73-OR strain adhesion and invasion were significantly reduced in TLR2^−/− A549 cells. Moreover, the lung clearance rate of the 73-OR strain was significantly higher in TLR2^−/− C57/BL6J mice than in wild-type (WT) mice. Histological analysis showed that inflammatory responses were milder in TLR2^−/− C57/BL6J mice than in WT mice, which was confirmed by a decrease in cytokine levels in TLR2^−/− C57/BL6J mice. Overall, these results indicate that TLR2 promoted M. catarrhalis adhesion and invasion of A549 cells and lung tissues and mediated inflammatory responses in infected lungs. This study provides important insights into the development of potential therapeutic strategies against M. catarrhalis and TLR2-induced inflammatory responses.

KEYWORDS:

• Moraxella catarrhalis
• alveolar epithelial cells
• adhesion
• invasion
• toll-like receptor 2

Disclosure statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Author contributions

Y.L. and Y.X. designed the study. R.D. and Y.L. wrote the paper. J.Y. and W.K. performed and analysed most of the experiments. L.D. and S.H. helped with the animals’ experiments.

Data Availability statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.

Correction Statement

This article has been corrected with minor changes. These changes do not impact the academic content of the article.

Additional information

Funding

This study was funded by grants from Beijing Natural Science Foundation (Youth Project) (Grant No. 7214245) and the National Natural Science Foundation of China (Grant No. 82102414).