IFN-β促进巨噬细胞细胞分泌IL-6参与干燥综合征相关肺间质病变

目的 探讨β-干扰素(IFN-β)在干燥综合征(SS)相关肺间质病变(SS-ILD)的作用及机制。方法 采用ELISA法检测血浆中IFN-β水平，分析SS患者IFN-β与EULAR干燥综合征疾病活动性指数(ESSDAI)的相关性，比较SS患者与健康人对照组IFN-β水平、SS-ILD与未伴ILD的SS患者血浆中IFN-β水平；用40 pg/mL重组人IFN-β处理人巨噬细胞24 h,用逆转录PCR法检测巨噬细胞白细胞介素6(IL-6) mRNA,用ELISA法检测巨噬细胞分泌IL-6蛋白水平；用ELISA法检测SS-ILD与未伴ILD的SS患者血浆中IL-6浓度，分析SS-ILD患者IL-6与IFN-β的相关性。结果 血浆IFN-β水平在SS患者中明显高于正常对照者(P<0.05),而且与疾病活动度呈显著正相关(P<0.05);SS-ILD患者较未伴有ILD的SS患者血浆IFN-β增高(P<0.05);IFN-β促进培养人巨噬细胞分泌IL-6;SS-ILD患者较未伴有ILD的SS患者血浆IL-6增高(P<0.05),SS-ILD患者IL-6水平与IFN-β呈正相...

IFN-β induced IL-6 production by macrophages in Sjogren′s syndrome-related interstitial lung disease

Objective To investigate the role and mechanism of interferon-β(IFN-β)in Sjogren′s syndrome-related interstitial lung disease(SS-ILD).Methods IFN-βin plasma was detected by an enzyme-linked immunosorbent assay(ELISA).The relationship between plasma IFN-βand EULAR Sjogren′s syndrome disease activity index(ESSDAI)in SS patients was analyzed.The plasma IFN-βlevels between SS patients and healthy controls and between SS patients with and without ILD were compared.Interleukin 6(IL-6)mRNA and protein levels in human macrophages treated with 40 pg/mL of recombinant human IFN-βfor 24 hours were detected by re-al-time PCR and ELISA,respectively.Plasma IL-6 levels in SS patients with ILD and without ILD were detected by ELISA,and the re-lationship between plasma IL-6 and IFN-βin SS-ILD patients was analyzed.Results Plasma IFN-βlevels in SS patients were signifi-cantly higher than that in healthy controls(P<0.05),and were positively correlated with disease activity of SS patients(P<0.05).Compared with SS patients without ILD,plasma IFN-βlevels in SS patients with ILD increased significantly(P<0.05).IFN-βpromo-ted cultured human macrophages to secrete IL-6.Plasma IL-6 levels in SS-ILD patients were significantly higher than that in SS patients without ILD(P<0.05),and were positively correlated with plasma IFN-βlevels.Conclusion IFN-βmay participate in or promote the occurrence of SS-ILD by inducing macrophages to secrete pro-inflammatory cytokine IL-6.