Effect of IL-6 on alveolar fibroblast proliferation in interstitial lung diseases

被引:58
作者
Shahar, I
Fireman, E
Topilsky, M
Grief, J
Kivity, S
Spirer, Z
BenEfraim, S
机构
[1] TEL AVIV UNIV,TEL AVIV MED CTR,ALLERGY CTR,IL-69978 TEL AVIV,ISRAEL
[2] TEL AVIV UNIV,TEL AVIV MED CTR,DEPT INTERNAL MED E,IL-69978 TEL AVIV,ISRAEL
[3] TEL AVIV UNIV,TEL AVIV MED CTR,DANA CHILDRENS HOSP,IL-69978 TEL AVIV,ISRAEL
[4] TEL AVIV UNIV,SACKLER FAC MED,DEPT HUMAN MICROBIOL,IL-69978 TEL AVIV,ISRAEL
来源
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY | 1996年 / 79卷 / 03期
关键词
D O I
10.1006/clin.1996.0075
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Alveolar macrophage-fibroblast interaction may be involved in the pathogenesis of interstitial lung diseases (ILD). Herein, we compared IL-6 secretion hom alveolar macrophages (AM) and alveolar fibroblasts (AFb) recovered from patients with sarcoidosis (SA) and with diffuse interstitial fibrosis (DIF). Moreover, we evaluated the effect of IL-6 on the in vitro AFb proliferation in both diseases. AM and AFb from SA patients showed increased spontaneous secretion of IL-6 compared with cells from DH subjects. Tumor necrosis factor-alpha (TNF alpha) and interleukin-1 (IL-1) enhanced IL-6 secretion and IL-6 mRNA transcription in AFb of SA patients. Addition of anti-IL-g MoAbs increased AFb proliferation capacity in SA, but suppressed it in DIF. These results show that only SA AM and AFb secrete high levels of IL-6 which have suppressive effect on AFb proliferation. This may indicate a potential role of IL-6 in the fibrogenesis of ILD. (C) 1996 Academic Press, Inc.
引用
收藏
页码:244 / 251
页数:8
相关论文
共 23 条
[1]  
BREEN E, 1990, J BIOL CHEM, V265, P6286
[2]   IMMUNOLOGY OF SARCOIDOSIS [J].
DANIELE, RP .
SEMINARS IN RESPIRATORY MEDICINE, 1991, 12 (03) :204-214
[3]   INTERLEUKIN-6 IN MOUSE HYPERSENSITIVITY PNEUMONITIS - CHANGES IN LUNG FREE-CELLS FOLLOWING DEPLETION OF ENDOGENOUS IL-6 OR DIRECT ADMINISTRATION OF IL-6 [J].
DENIS, M .
JOURNAL OF LEUKOCYTE BIOLOGY, 1992, 52 (02) :197-201
[4]   FIBROBLAST INTERLEUKIN 1-BETA - SYNERGISTIC STIMULATION BY RECOMBINANT INTERLEUKIN-1 AND TUMOR NECROSIS FACTOR AND POSTTRANSCRIPTIONAL REGULATION [J].
ELIAS, JA ;
REYNOLDS, MM ;
KOTLOFF, RM ;
KERN, JA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1989, 86 (16) :6171-6175
[5]  
Fireman E, 1992, Mediators Inflamm, V1, P319, DOI 10.1155/S0962935192000474
[6]   CELL-FREE SUPERNATANTS OF SARCOID ALVEOLAR MACROPHAGES SUPPRESS PROLIFERATION OF SARCOID ALVEOLAR FIBROBLASTS [J].
FIREMAN, E ;
BENEFRAIM, S ;
MESSER, G ;
DABUSH, S ;
GREIF, J ;
TOPILSKY, M .
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY, 1991, 59 (03) :368-378
[7]  
FIREMAN E, 1988, IMMUNL LETT, V181, P159
[8]   INTERLEUKIN-6 IS AN AUTOCRINE GROWTH-FACTOR FOR MURINE LUNG FIBROBLAST SUBSETS [J].
FRIES, KM ;
FELCH, ME ;
PHIPPS, RP .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 1994, 11 (05) :552-560
[9]  
HUNNINGHAKE GW, 1984, AM REV RESPIR DIS, V130, P476
[10]   RADIATION-INDUCED CHANGES IN LUNG-TISSUE AND DEVELOPMENT OF FIBROSIS DETERMINED BY QUANTITATIVE MORPHOMETRIC METHODS [J].
KRAUS, R ;
STEINBERG, F ;
REHN, B ;
BRUCH, J ;
STREFFER, C .
JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY, 1991, 117 (01) :27-32