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

Publisher: Taylor & Francis Country of Publication: United States NLM ID: 101531386 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2150-5608 (Electronic) Linking ISSN: 21505594 NLM ISO Abbreviation: Virulence Subsets: MEDLINE

Publication: 2015- : Philadelphia, PA : Taylor & Francis
Original Publication: Austin, Tex. : Landes Bioscience

Alveolar Epithelial Cells* ; Toll-Like Receptor 2*/genetics; Animals ; Mice ; Epithelial Cells ; Lung ; Moraxella catarrhalis/genetics

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.

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7214245 Beijing Natural Science Foundation (Youth Project; 82102414 National Natural Science Foundation of China

Keywords: Moraxella catarrhalis; adhesion; alveolar epithelial cells; invasion; toll-like receptor 2

0 (Toll-Like Receptor 2)
0 (Tlr2 protein, mouse)

Date Created: 20240103 Date Completed: 20240109 Latest Revision: 20240517

20240517

PMC10772937

10.1080/21505594.2023.2298548

38169345