SPLUNC1 regulation in airway epithelial cells: role of toll-like receptor 2 signaling View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2010-12

AUTHORS

Hong Wei Chu, Fabienne Gally, Jyoti Thaikoottathil, Yvonne M Janssen-Heininger, Qun Wu, Gongyi Zhang, Nichole Reisdorph, Stephanie Case, Maisha Minor, Sean Smith, Di Jiang, Nicole Michels, Glenn Simon, Richard J Martin

ABSTRACT

BACKGROUND: Respiratory infections including Mycoplasma pneumoniae (Mp) contribute to various chronic lung diseases. We have shown that mouse short palate, lung, and nasal epithelium clone 1 (SPLUNC1) protein was able to inhibit Mp growth. Further, airway epithelial cells increased SPLUNC1 expression upon Mp infection. However, the mechanisms underlying SPLUNC1 regulation remain unknown. In the current study, we investigated if SPLUNC1 production following Mp infection is regulated through Toll-like receptor 2 (TLR2) signaling. METHODS: Airway epithelial cell cultures were utilized to reveal the contribution of TLR2 signaling including NF-κB to SPLUNC1 production upon bacterial infection and TLR2 agonist stimulation. RESULTS: Mp and TLR2 agonist Pam3CSK4 increased SPLUNC1 expression in tracheal epithelial cells from wild type, but not TLR2(-/-) BALB/c mice. RNA interference (short-hairpin RNA) of TLR2 in normal human bronchial epithelial cells under air-liquid interface cultures significantly reduced SPLUNC1 levels in Mp-infected or Pam3CSK4-treated cells. Inhibition and activation of NF-κB pathway decreased and increased SPLUNC1 production in airway epithelial cells, respectively. CONCLUSIONS: Our data for the first time suggest that airway epithelial TLR2 signaling is pivotal in mycoplasma-induced SPLUNC1 production, thus improving our understanding of the aberrant SPLUNC1 expression in airways of patients suffering from chronic lung diseases with bacterial infections. More... »

PAGES

155

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/1465-9921-11-155

DOI

http://dx.doi.org/10.1186/1465-9921-11-155

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1033254428

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/21054862


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