Effect of IL-6 on alveolar fibroblast proliferation in interstitial lung diseases.
Alveolar macrophage-fibroblast interaction may be involved in the pathogenesis of interstitial lung diseases (ILD). Herein, we compared IL-6 secretion from 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 DIF subjects. Tumor necrosis factor-alpha (TNFalpha) and interleukin-1 (IL-1) enhanced IL-6 secretion and IL-6 mRNA transcription in AFb of SA patients. Addition of anti-IL-6 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.
Shahar
I
I
Department of Pulmonary Diseases and Allergy Center, Tel-Aiv Medical Center, Israel.
Fireman
E
E
Topilsky
M
M
Grief
J
J
Kivity
S
S
Spirer
Z
Z
Ben Efraim
S
S
D002455:Cell Division / Q000187:drug effects; D005347:Fibroblasts / Q000166:cytology; D015870:Gene Expression; D006801:Humans; D007375:Interleukin-1 / Q000494:pharmacology; D015850:Interleukin-6 / Q000502:physiology*; D017563:Lung Diseases, Interstitial / Q000378:metabolism / Q000473:pathology*; D016676:Macrophages, Alveolar / Q000502:physiology; D011650:Pulmonary Alveoli / Q000166:cytology*; D012333:RNA, Messenger / Q000378:metabolism; D012507:Sarcoidosis / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
D007375:Interleukin-1; D015850:Interleukin-6; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha