HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Yasutomi, M. Articles by Mayumi, M. Search for Related Content PubMed PubMed Citation Articles by Yasutomi, M. Articles by Mayumi, M. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB ERYTHROMYCIN

Erythromycin Differentially Inhibits Lipopolysaccharide- or Poly(I:C)-Induced but Not Peptidoglycan-Induced Activation of Human Monocyte-Derived Dendritic Cells¹

Motoko Yasutomi^*, Yusei Ohshima^2,*, Nemuko Omata^*, Akiko Yamada^*, Hiromichi Iwasaki, Yoshimasa Urasaki and Mitsufumi Mayumi^*

^* Department of Pediatrics, Faculty of Medical Sciences, University of Fukui, Fukui, Japan; and Division of Transfusion Medicine, Fukui Medical University Hospital, Fukui, Japan

Erythromycin (EM) has attracted attention because of its anti-inflammatory effect. Because dendritic cells (DCs) are the most potent APCs involved in numerous pathologic processes including innate immunity, we examined effects of EM on the activation of human DCs by pathogen-derived stimuli. Monocyte-derived DCs were pretreated with EM and subsequently stimulated with peptidoglycan, polyriboinosinic:polyribocytidylic acid (poly(I:C)), or LPS. The activation of DCs was assessed by surface molecule expression and cytokine production. To reveal the signaling pathways affected by EM, TLR expression, NF-B, IFN regulatory factor-3, and AP-1 activation were examined. EM inhibited costimulatory molecule expression and cytokine production that was induced by poly(I:C) and LPS but not by peptidoglycan. EM pretreatment down- and up-regulated mRNA levels of TLR3 and TLR2, respectively, but did not affect that of TLR4. EM suppressed IFN regulatory factor-3 activation and IFN- production but not AP-1 activation induced by poly(I:C) and LPS. The inhibitory effect of EM on NF-B activation was observed only in poly(I:C)-stimulated DCs. EM selectively suppressed activation of DCs induced by LPS and poly(I:C) in different ways, suggesting that the immuno-modulating effects of EM depend on the nature of pathogens. These results might explain why EM prevents the virus-induced exacerbation in the chronic inflammatory respiratory diseases and give us the clue to design new drugs to treat these diseases.

This article has been cited by other articles:

				K. Ikeda, K. Tojo, Y. Inada, Y. Takada, M. Sakamoto, M. Lam, W. C Claycomb, and N. Tajima Regulation of urocortin I and its related peptide urocortin II by inflammatory and oxidative stresses in HL-1 cardiomyocytes J. Mol. Endocrinol., June 1, 2009; 42(6): 479 - 489. [Abstract] [Full Text] [PDF]