title: Effects of the macrolide antibiotic, midecamycin, on Staphylococcus aureus product-induced Th2 cytokine response in patients with atopic dermatitis.
abstract: In the present study, the effects of the macrolide antibiotic, midecamycin (MDM), on the Th2 cytokine response induced by the Staphylococcus aureus products, staphylococcal enterotoxin B (SEB), lipoteichoic acid (LTA), and peptidoglycan (PEG), was investigated in human peripheral blood mononuclear cells (PBMCs) from patients with atopic dermatitis (AD). MDM inhibited SEB-induced mRNA expression of the Th2 cytokines interleukin-4 (IL-4) and IL-5 in PBMCs from patients with AD. Furthermore, MDM also suppressed LTA-induced or PEG-induced IL-5 mRNA expression in these patients. Inhibition of mRNA expression by MDM correlated with the synthesis of cytokines in PBMCs, indicating that MDM controls Th2 cytokine production. In addition, S. aureus strains isolated from skin lesions of patients with AD were particularly susceptible to MDM compared with gentamicin, which is used widely in Japan as an antibiotic ointment combined with steroid for topical application in AD. These results suggest that topical administration of MDM might be beneficial in AD lesions infected with S. aureus.
authors.affiliation: Department of Immunobiology, Meiji Pharmaceutical University, Kiyose, Tokyo 204-8588, Japan. kmatsui@my-pharm.ac.jp
authors.forename: Katsuhiko
authors.initials: K
authors.lastname: Matsui
authors.forename: Akemi
authors.initials: A
authors.lastname: Nishikawa
mesh_terms: D000328:Adult; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D016207:Cytokines / Q000096:biosynthesis* / Q000235:genetics; D003876:Dermatitis, Atopic / Q000276:immunology*; D004768:Enterotoxins / Q000037:antagonists & inhibitors; D005786:Gene Expression Regulation; D005839:Gentamicins / Q000494:pharmacology; D006801:Humans; D015847:Interleukin-4 / Q000096:biosynthesis / Q000235:genetics; D015848:Interleukin-5 / Q000096:biosynthesis / Q000235:genetics; D007933:Leucomycins / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000037:antagonists & inhibitors; D018942:Macrolides / Q000494:pharmacology; D010457:Peptidoglycan / Q000494:pharmacology; D012333:RNA, Messenger / Q000096:biosynthesis; D013211:Staphylococcus aureus / Q000378:metabolism / Q000502:physiology*; D013682:Teichoic Acids / Q000037:antagonists & inhibitors; D018418:Th2 Cells / Q000187:drug effects* / Q000276:immunology
chemical_list: D000900:Anti-Bacterial Agents; D016207:Cytokines; D004768:Enterotoxins; D005839:Gentamicins; D015848:Interleukin-5; D007933:Leucomycins; D008070:Lipopolysaccharides; D018942:Macrolides; D010457:Peptidoglycan; D012333:RNA, Messenger; D013682:Teichoic Acids; D015847:Interleukin-4; C031818:enterotoxin B, staphylococcal; C009900:lipoteichoic acid; C026483:midecamycin