ERYTHROMYCIN SUPPRESSES INTERLEUKIN-6 EXPRESSION BY HUMAN BRONCHIAL EPITHELIAL-CELLS - A POTENTIAL MECHANISM OF ITS ANTIINFLAMMATORY ACTION

被引：111

作者：

TAKIZAWA, H ^{[1
]}

DESAKI, M ^{[1
]}

OHTOSHI, T ^{[1
]}

KIKUTANI, T ^{[1
]}

OKAZAKI, H ^{[1
]}

SATO, M ^{[1
]}

AKIYAMA, N ^{[1
]}

SHOJI, S ^{[1
]}

HIRAMATSU, K ^{[1
]}

ITO, K ^{[1
]}

机构：

[1] JUNTENDO UNIV, SCH MED, DEPT BACTERIOL, BUNKYO KU, TOKYO 113, JAPAN

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 1995年 / 210卷 / 03期

关键词：

D O I：

10.1006/bbrc.1995.1727

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

We evaluated the effects of several antibiotics on IL-6 expression by human bronchial epithelial cells, potent sources of this proinflammatory tory cytokine important in airway inflammation. Among those tested, erythromycin (EM) and clarithromycin (CAM) uniquely suppressed mRNA levels as well as the release of IL-6 at the therapeutic and non-cytotoxic concentration (10(-6)M). Our findings suggested that these macrolide antibiotics had suppressive effect on cytokine expression in human cells, and this new mode of action may have relevance to their clinical effectiveness in airway inflammatory diseases. (C) 1995 Academic Press, Inc.

引用

页码：781 / 786

页数：6

共 20 条

[1] CYTOKINES AS MEDIATORS OF CHRONIC ASTHMA [J].

BARNES, PJ .

AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1994, 150 (05) :S42-S49

[2] CYTOKINES IN SYMPTOMATIC ASTHMA AIRWAYS [J].

BROIDE, DH ;

LOTZ, M ;

CUOMO, AJ ;

COBURN, DA ;

FEDERMAN, EC ;

WASSERMAN, SI .

JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 1992, 89 (05) :958-967

[3]

CHOMCZYNSKI P, 1987, ANAL BIOCHEM, V162, P156, DOI 10.1016/0003-2697(87)90021-2

[4] COMPLEMENTARY-DNA FOR A NOVEL HUMAN INTERLEUKIN (BSF-2) THAT INDUCES LYMPHOCYTES-B TO PRODUCE IMMUNOGLOBULIN [J].

HIRANO, T ;

YASUKAWA, K ;

HARADA, H ;

TAGA, T ;

WATANABE, Y ;

MATSUDA, T ;

KASHIWAMURA, S ;

NAKAJIMA, K ;

KOYAMA, K ;

IWAMATSU, A ;

TSUNASAWA, S ;

SAKIYAMA, F ;

MATSUI, H ;

TAKAHARA, Y ;

TANIGUCHI, T ;

KISHIMOTO, T .

NATURE, 1986, 324 (6092) :73-76

[5] ERYTHROMYCIN DOES NOT DIRECTLY AFFECT NEUTROPHIL FUNCTIONS [J].

HOJO, I ;

FUJITA, I ;

HAMASAKI, Y ;

MIYAZAKI, M ;

MIYAZAKI, S .

CHEST, 1994, 105 (02) :520-523

[6] USE OF MACROLIDE ANTIBIOTIC SUBSTANCES IN TREATMENT OF ASTHMA [J].

ITKIN, IH ;

MENZEL, ML .

JOURNAL OF ALLERGY, 1970, 45 (03) :146-&

[7] A MECHANISM OF ERYTHROMYCIN TREATMENT IN PATIENTS WITH DIFFUSE PANBRONCHIOLITIS [J].

KADOTA, J ;

SAKITO, O ;

KOHNO, S ;

SAWA, H ;

MUKAE, H ;

ODA, H ;

KAWAKAMI, K ;

FUKUSHIMA, K ;

HIRATANI, K ;

HARA, K .

AMERICAN REVIEW OF RESPIRATORY DISEASE, 1993, 147 (01) :153-159

[8] ANTILYMPHOCYTIC ACTIVITY OF ERYTHROMYCIN DISTINCT FROM THAT OF FK506 OR CYCLOSPORINE-A [J].

KEICHO, N ;

KUDOH, S ;

YOTSUMOTO, H ;

AKAGAWA, KS .

JOURNAL OF ANTIBIOTICS, 1993, 46 (09) :1406-1413

[9] ERYTHROMYCIN PROMOTES MONOCYTE TO MACROPHAGE DIFFERENTIATION [J].

KEICHO, N ;

KUDOH, S ;

YOTSUMOTO, H ;

AKAGAWA, KS .

JOURNAL OF ANTIBIOTICS, 1994, 47 (01) :80-89

[10] ERYTHROMYCIN AND ITS DERIVATIVES WITH MOTILIN-LIKE BIOLOGICAL-ACTIVITIES INHIBIT THE SPECIFIC BINDING OF I-125 MOTILIN TO DUODENAL MUSCLE [J].

KONDO, Y ;

TORII, K ;

OMURA, S ;

ITOH, Z .

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1988, 150 (02) :877-882

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