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

被引:57
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