Published ahead of print on July 8, 2004, doi:10.1165/rcmb.2004-0161OC Am. J. Respir. Cell Mol. Biol., Volume 31, Number 4, October 2004, 463-469 A more recent version of this article appeared on October 1, 2004
Submitted on May 12, 2004 Corticosteroid and cytokines synergistically enhance TLR2 expression in respiratory epithelial cellsToshiki Homma1,1 Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo, Japan, 2 Division of Allergy, National Center for Child Health and Development, Tokyo, Japan, 3 Department of Otorhinolaryngology, Jikei Medical School, Tokyo, Japan, 4 Department of Microbiology, Kochi Medical School, Kochi, Japan, 5 Department of Pediatrics, Kochi Medical School, Kochi, Japan, 6 Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo, Japan; Research Team for Allergy Transcriptome, RIKEN Research Center for Allergy and Immunology, Yokohama, Japan * To whom correspondence should be addressed. E-mail: kmatsumoto{at}nch.go.jp.
Respiratory epithelial cells play important roles not only in host defense mechanisms but also in inflammatory responses. Inhaled corticosteroids are widely used for the treatment of patients with inflammatory lung disorders including asthma, chronic obstructive pulmonary disease and sarcoidosis. Corticosteroids effectively reduce the production of inflammatory mediators such as cytokines and chemokines. Though these molecules are also essential for host defense responses, there is no convincing evidence that inhaled corticosteroids increase susceptibility to lower respiratory tract infections. To test the involvement of Toll-like receptor (TLR) family molecules in this phenomenon, we examined the effects of various cytokines and corticosteroid on the expression of TLRs in human respiratory epithelial cells. Among the TLRs tested, TLR2 expression was significantly enhanced after stimulation with a combination of TNF-
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and IFN-
. Dexamethasone synergistically enhanced TLR2 expression in combination with TNF-
-defensin-2 after stimulation with peptidoglycan. These results provide evidence for a novel function of corticosteroids in airway inflammatory disorders and indicate that the use of inhaled corticosteroids in such disorders may have a beneficial role in host defense mechanisms.
