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Mycoplasma pneumoniae induces airway epithelial cell expression of MUC5AC in asthma

¹ Dept of Medicine and Surgery, Duke University Medical Center, Durham, ² Dept of Molecular Biomedical Sciences, North Carolina State University, Raleigh, NC, ³ Dept of Pediatrics, University of Alabama, Birmingham, AL, ⁵ Dept of Medicine, National Jewish Medical and Research Center, Denver, CO, and ⁴ Dept of Microbiology, University of Georgia, Athens, GA, USA.

CORRESPONDENCE: M. Kraft, Duke University Medical Center, MSRB M275, Research Drive, Durham, NC 27710, USA. Fax: 1 9196848408. E-mail: monika.kraft{at}duke.edu

Keywords: Asthma, epithelial cell, MUC5AC, Mycoplasma pneumoniae, toll-like receptor 2

Received: August 9, 2007
Accepted September 21, 2007

As excess mucin expression can contribute to the exacerbation of asthma, the present authors hypothesised that Mycoplasma pneumoniae significantly induces MUC5AC (the major airway mucin) expression in airway epithelial cells isolated directly from asthmatic subjects.

A total of 11 subjects with asthma and six normal controls underwent bronchoscopy with airway brushing. Epithelial cells were cultured at an air–liquid interface and incubated with and without M. pneumoniae for 48 h, and in the presence and absence of nuclear factor (NF)-B and a toll-like receptor (TLR)2 inhibitor. Quantitative PCR was performed for MUC5AC and TLR2 mRNA. MUC5AC protein and total protein were determined by ELISA.

M. pneumoniae exposure significantly increased MUC5AC mRNA and protein expression after 48 h in epithelial cells isolated from asthmatic, but not from normal control subjects, at all concentrations as compared to unexposed cells. TLR2 mRNA expression was significantly increased in asthmatic epithelial cells at 4 h compared with unexposed cells. NF-B and TLR2 inhibition reduced MUC5AC expression to the level of the unexposed control in both groups.

Mycoplasma pneumoniae exposure significantly increased MUC5AC mRNA and protein expression preferentially in airway epithelial cells isolated from asthmatic subjects. The toll-like receptor 2 pathway may be involved in this process.