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

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14 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)260-268
Number of pages9
JournalActa Tropica
Volume105
Issue number3
DOIs
Publication statusPublished - Mar 2008

Fingerprint

Toxocara canis
transforming growth factor beta 1
transforming growth factors
hepatitis
Transforming Growth Factors
Transforming Growth Factor beta
smooth muscle
Hepatitis
Smooth Muscle Myocytes
actin
collagen
Actins
Hepatic Stellate Cells
Collagen
mice
liver
lesions (animal)
leukocytes
Leukocytes
cells

Keywords

  • α-Smooth muscle actins
  • Collagen
  • Granulomatous hepatitis
  • Immunohistochemistry
  • Mice
  • Stellate cells
  • Toxocara canis
  • Transforming growth factor-β1

ASJC Scopus subject areas

  • Parasitology
  • Infectious Diseases

Cite this

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title = "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",
abstract = "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.",
keywords = "α-Smooth muscle actins, Collagen, Granulomatous hepatitis, Immunohistochemistry, Mice, Stellate cells, Toxocara canis, Transforming growth factor-β1",
author = "Wu, {Ming Shun} and Liao, {Chien Wei} and Du, {Wen Yun} and Kao, {Ting Chang} and Su, {Kua Eyre} and Lin, {Yun Ho} and Chang, {Chun Chao} and Fan, {Chia Kwung}",
year = "2008",
month = "3",
doi = "10.1016/j.actatropica.2007.11.005",
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T1 - 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

AU - Wu, Ming Shun

AU - Liao, Chien Wei

AU - Du, Wen Yun

AU - Kao, Ting Chang

AU - Su, Kua Eyre

AU - Lin, Yun Ho

AU - Chang, Chun Chao

AU - Fan, Chia Kwung

PY - 2008/3

Y1 - 2008/3

N2 - 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.

AB - 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.

KW - α-Smooth muscle actins

KW - Collagen

KW - Granulomatous hepatitis

KW - Immunohistochemistry

KW - Mice

KW - Stellate cells

KW - Toxocara canis

KW - Transforming growth factor-β1

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U2 - 10.1016/j.actatropica.2007.11.005

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VL - 105

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EP - 268

JO - Acta Tropica

JF - Acta Tropica

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