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血吸虫卵肉芽肿衍生的成纤维细胞刺激因子明显不同于白细胞介素-1。

Schistosomal egg granuloma-derived fibroblast-stimulating factor is apparently distinct from interleukin-1.

作者信息

Prakash S, Dinarello C A, Danko K, Stadecker M J, Wyler D J

机构信息

Department of Medicine, New England Medical Center Hospitals, Boston, Massachusetts.

出版信息

Infect Immun. 1989 Mar;57(3):679-84. doi: 10.1128/iai.57.3.679-684.1989.

Abstract

We have previously reported that egg granulomas isolated from livers of Schistosoma mansoni-infected euthymic mice in vitro elaborate a factor(s) that stimulates a variety of fibroblast responses including fibroblast proliferation and enhanced synthesis of extracellular matrix proteins. We have postulated that these factors play a role in the pathogenesis of hepatic fibrosis in schistosomiasis mansoni. Serum-free supernatants from egg granuloma cultures also stimulate thymocyte proliferation in an assay that defects interleukin-1 (IL-1). Thymocytes and fibroblasts are stimulated to proliferate by the same fractions of egg granuloma culture supernatant separated by gel filtration, isoelectric focusing, and ion-exchange chromatography. This suggested that granuloma-derived IL-1 is responsible for the observed fibroblast stimulation. Here we report that the ability of granuloma culture supernatants to stimulate the IL-1-sensitive D10.G4.1 cells but not fibroblasts is removed by treatment with immobilized anti-IL-1 antibody. We also observed that dialyzed culture supernatants from egg granulomas obtained from infected congenitally athymic (nude) mice also stimulate fibroblast proliferation. Treatment with anti-IL-1 antibody did not abrogate this response. In contrast to our experience with egg granulomas isolated from euthymic mice, IL-1- and fibroblast-stimulating activity could be separated by gel filtration and isoelectric focusing. We conclude that the fibroblast growth-stimulating activities elaborated by egg granulomas from S. mansoni-infected euthymic and athymic mice may be different but both appear to be distinct from IL-1.

摘要

我们之前报道过,从感染曼氏血吸虫的正常小鼠肝脏中分离出的虫卵肉芽肿在体外可产生一种因子,该因子能刺激多种成纤维细胞反应,包括成纤维细胞增殖以及细胞外基质蛋白合成的增强。我们推测这些因子在曼氏血吸虫病肝纤维化的发病机制中起作用。虫卵肉芽肿培养物的无血清上清液在检测白细胞介素 -1(IL-1)的实验中也能刺激胸腺细胞增殖。胸腺细胞和成纤维细胞可被经凝胶过滤、等电聚焦和离子交换色谱分离的虫卵肉芽肿培养上清液的相同组分刺激增殖。这表明肉芽肿来源的IL-1是观察到的成纤维细胞刺激的原因。在此我们报道,用固定化抗IL-1抗体处理可消除肉芽肿培养上清液刺激IL-1敏感的D10.G4.1细胞而非成纤维细胞的能力。我们还观察到,从先天性无胸腺(裸)感染小鼠获得的虫卵肉芽肿的透析培养上清液也能刺激成纤维细胞增殖。用抗IL-1抗体处理并未消除这种反应。与我们从正常小鼠分离出的虫卵肉芽肿的经验不同,IL-1和成纤维细胞刺激活性可通过凝胶过滤和等电聚焦分离。我们得出结论,来自感染曼氏血吸虫的正常和无胸腺小鼠的虫卵肉芽肿所产生的成纤维细胞生长刺激活性可能不同,但两者似乎都与IL-1不同。

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Macrophage-derived growth factor for fibroblasts and Interleukin-1 are distinct entities.
J Leukoc Biol. 1984 Jan;35(1):115-29. doi: 10.1002/jlb.35.1.115.
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Interleukin-1.白细胞介素-1
Rev Infect Dis. 1984 Jan-Feb;6(1):51-95. doi: 10.1093/clinids/6.1.51.

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