Publications (2)3.88 Total impact
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Article: Hepatitis B virus particles preferably induce Kupffer cells to produce TGF-β1 over pro-inflammatory cytokines.
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ABSTRACT: Kupffer cells and related cytokines are thought to play a critical role in liver fibrosis; however, the role played by Kupffer cells in hepatitis B virus-related fibrogenesis is unknown. Primary rat Kupffer cells were cultured with different titres of hepatitis B virus particles and the concentrations of transforming growth factor (TGF)-β1, interleukin (IL)-1, IL-6 and tumour necrosis factor (TNF)-α in the culture supernatant were measured every 24h for 7 days. The mRNA and protein levels of these cytokines in Kupffer cells were also analysed using quantitative real-time polymerase chain reaction and western blotting, respectively. Kupffer cells maintained normal morphology and function throughout the 7-day exposure to hepatitis B virus. The concentration of TGF-β1 secreted by hepatitis B virus-stimulated Kupffer cells (6 log IU/ml hepatitis B virus) increased 5.38- and 7.75-fold by Days 3 and 7, respectively (p<0.01). Western blotting showed that TGF-β1 expression in Kupffer cells exposed to high titres of hepatitis B virus increased 1.80- and 2.42-fold by Days 3 and 7, respectively (p<0.01). In contrast, Kupffer cell expression and secretion of pro-inflammatory cytokines (IL-6, IL-1 and TNF-α) was unchanged throughout the experiment. Hepatitis B virus preferentially stimulates Kupffer cells to produce the pro-fibrogenic/anti-inflammatory cytokine TGF-β1 rather than the pro-inflammatory cytokines IL-6, IL-1 and TNF-α. This may partly explain why overt liver fibrosis still presents in cases of chronic hepatitis B virus infection with minimal (or no) necro-inflammation.Digestive and Liver Disease 12/2011; 44(4):328-33. · 3.05 Impact Factor -
Article: Rat renal interstitial fibroblasts affect the TH1/TH2 profile in vitro.
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ABSTRACT: T helper 1 (Th1)/T helper 2 (Th2) profile is pivotal in the development of fibrosis. Renal interstitial fibroblasts, which play a central role in the development of renal interstitial fibrosis, have an intimate relation with lymphocytes. However, there is little knowledge of the effect of fibroblasts on the profile of CD4 T-lymphocyte subsets. After coculture with rat renal interstitial fibroblasts, the proportions of Th1 and Th2 cells in CD4 T lymphocytes and the apoptosis rates of the two subsets were detected by flow cytometry. Galectin-9 expression in rat renal interstitial fibroblasts was detected by immunofluorescence, Western blotting, and enzyme-linked immunosorbent assay. After 48 h of coculture, rat renal interstitial fibroblasts increased the proportion of Th2 cells, lowering the ratio of Th1/Th2. Meanwhile, interferon-gamma production in Th1 cells was inhibited and interleukin-4 production in Th2 was promoted. After coculture with activated rat renal interstitial fibroblasts for 24 h, apoptosis of Th1 was more highly promoted than that of Th2 cells. In addition, rat renal interstitial fibroblasts induced stronger Th2 cell differentiation than that of Th1 cells in vitro. Rat renal interstitial fibroblasts expressed but did not secrete galectin-9 (an apoptosis-inducing factor for Th1 cells) in vitro and the expression level decreased when cocultured with CD4 T lymphocytes. Rat renal interstitial fibroblasts shift the Th1/Th2 profile in vitro, and this may be another pathway by which renal interstitial fibroblasts promote fibrosis.Renal Failure 01/2011; 33(10):1025-31. · 0.82 Impact Factor
