Enhanced expression of transforming growth factor-β1 in inflammatory cells, α-smooth muscle actin in stellate cells, and collagen accumulation in experimental granulomatous hepatitis caused by Toxocara canis in mice

Ming Shun Wu, Chien Wei Liao, Wen Yun Du, Ting Chang Kao, Kua Eyre Su, Yun Ho Lin, Chun Chao Chang, Chia Kwung Fan

研究成果: 雜誌貢獻文章同行評審

14 引文 斯高帕斯(Scopus)

摘要

Although toxocaral granulomatous hepatitis (TGH) characterized with a dominant-Th2 type immune response is a self-limiting disease, little is known concerning the role of fibrosis-related cytokine transforming growth factor-beta 1 (TGF-β1) in pathogenesis of TGH. A detailed histological and quantitatively immunohistochemical analysis of TGF-β1, α-smooth muscle actins (α-SMA), and collagen was performed on the liver tissues from mice infected with Toxocara canis as assessed between day 1 and 42 weeks post-infection (DPI or WPI). TGF-β1 was detected mainly in infiltrating leukocytes in lesions with strong expressions from 4 to 16 WPI. Larvae per se also exhibited strong TGF-β1-like molecule expressions in the trial. Alpha-SMA was detected predominantly in hepatic stellate cells (HSC) which surrounded the lesions with moderate expressions largely throughout the period of the entire experiment. Collagen was observed to accumulate in inflammatory lesions and biliary basement with moderate to strong expressions from 1 WPI onwards in the trial. Since many evidences have indicated that leukocytes have the potential to influence HSC by producing TGF-β1 which can affect HSC to increase collagen synthesis in various liver diseases, we may propose that persistently elevated TGF-β1 expression in infiltrating leukocytes and active HSC with marked α-SMA expressions may contribute to healing of injured sites through up-stimulation of collagen deposition; in contrast, abnormally persistent collagen accumulation may cause irreversible fibrotic injury in the TGH.
原文英語
頁(從 - 到)260-268
頁數9
期刊Acta Tropica
105
發行號3
DOIs
出版狀態已發佈 - 三月 2008

ASJC Scopus subject areas

  • 寄生物學
  • 傳染性疾病

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