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FEMS Immunol Med Microbiol. 2009 Aug;56(3):233-40. doi: 10.1111/j.1574-695X.2009.00571.x. Epub 2009 May 21.

Low concentrations of LL-37 alter IL-8 production by keratinocytes and bronchial epithelial cells in response to proinflammatory stimuli.

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1
Department of Microbiology and Immunology, Centre for Microbial Diseases and Immunity Research, University of British Columbia, Lower Mall Research Station, Vancouver, BC, Canada V6T 1Z4.

Abstract

The immunomodulatory cationic host defence peptide LL-37 plays an important role in epithelial innate immunity; at higher concentrations (20-50 microg mL(-1)) associated with inflammation, LL-37 elicits the production of cytokines and chemokines. It was demonstrated here that lower, physiologically relevant LL-37 concentrations (2-3 microg mL(-1)) altered epithelial cell responses to proinflammatory stimuli. In combination with interleukin-1beta (IL-1beta) and the Toll-like receptor-5 (TLR5) agonist flagellin, these low concentrations of LL-37 synergistically increased IL-8 production by both proliferating and differentiated keratinocytes and by bronchial epithelial cells. In combination with the TLR2/1 agonist PAM3CSK4, LL-37 synergistically induced transcription and the release of both IL-8 and IL-6 from primary bronchial epithelial cells; the IL-8 response was demonstrated to be regulated by epidermal growth factor receptor signalling. Treatment of bronchial epithelial cells with LL-37 and the TLR3 agonist polyI:C resulted in synergistic increases in IL-8 release and cytotoxicity. These data indicate that low concentrations of LL-37 may alter epithelial responses to infecting microorganisms in vivo.

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