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TLR2 signaling is critical for Mycoplasma pneumoniae-induced airway mucin expression
Hong Wei Chu1, Samithamby Jeyaseelan, John G Rino
1Department of Medicine, National Jewish Medical and Research Center and University of Colorado Health Sciences Center, Denver, CO 80206, USA.
Abstract:
Excessive airway mucin production contributes to airway obstruction in lung diseases such as asthma and chronic obstructive pulmonary disease. Respiratory infections, such as atypical bacterium Mycoplasma pneumoniae (Mp), have been proposed to worsen asthma and chronic obstructive pulmonary disease in part through increasing mucin. However, the molecular mechanisms involved in infection-induced airway mucin overexpression remain to be determined. TLRs have been recently shown to be a critical component in host innate immune response to infections. TLR2 signaling has been proposed to be involved in inflammatory cell activation by mycoplasma-derived lipoproteins. In this study, we show that TLR2 signaling is critical in Mp-induced airway mucin expression in mice and human lung epithelial cells. Respiratory Mp infection in BALB/c mice activated TLR2 signaling and increased airway mucin. A TLR2-neutralizing Ab significantly reduced mucin expression in Mp-infected BALB/c mice. Furthermore, Mp-induced airway mucin was abolished in TLR2 gene-deficient C57BL/6 mice. Additionally, Mp was shown to increase human lung A549 epithelial cell mucin expression, which was inhibited by the overexpression of a human TLR2 dominant-negative mutant. These results clearly demonstrate that respiratory Mp infection increases airway mucin expression, which is dependent on the activation of TLR2 signaling.
Insights
Mycoplasma pneumoniae infection increases airway mucin, worsening lung diseases like asthma. This occurs via Toll-like receptor 2 (TLR2) signaling, a key part of the innate immune response.
Area of Science:
- Immunology
- Respiratory Medicine
- Microbiology
Background:
- Excessive airway mucin production is a hallmark of obstructive lung diseases.
- Respiratory infections, including Mycoplasma pneumoniae (Mp), may exacerbate these conditions by increasing mucin.
- The precise molecular mechanisms linking infection to mucin overexpression are not fully understood.
Purpose of the Study:
- To investigate the role of Toll-like receptor 2 (TLR2) signaling in Mycoplasma pneumoniae-induced airway mucin production.
- To elucidate the molecular pathways involved in infection-driven mucin overexpression.
Main Methods:
- Utilized BALB/c mice infected with Mp to assess airway mucin expression and TLR2 activation.
- Employed TLR2-neutralizing antibodies in infected mice.
- Investigated Mp effects on mucin in TLR2 gene-deficient mice.
- Examined Mp-induced mucin changes in human A549 lung epithelial cells, including the use of a dominant-negative TLR2 mutant.
Main Results:
- Respiratory Mp infection activated TLR2 signaling and significantly increased airway mucin in mice.
- Neutralization of TLR2 signaling reduced mucin levels in infected mice.
- Mp-induced airway mucin production was completely absent in TLR2 gene-deficient mice.
- Mp increased mucin expression in human lung epithelial cells, an effect inhibited by blocking TLR2 signaling.
Conclusions:
- Respiratory Mycoplasma pneumoniae infection leads to increased airway mucin expression.
- This mucin overexpression is critically dependent on the activation of Toll-like receptor 2 (TLR2) signaling.
- TLR2 plays a pivotal role in the innate immune response to Mp infection concerning airway mucin regulation.
