Abstract
Transforming growth factor (TGF-β1) is among the strongest factors of liver fibrogenesis, but its association with Schistosoma-caused liver fibrosis is controversial. Tissue transglutaminase (tTG) is the principal enzyme controlling TGF-β1 maturation and contributes to Sj-infected liver fibrosis. Here we aim to explore the consistency between tTG and TGF-β1 and TGF-β1 source and its correlation with liver fibrosis after Sj-infection. TGF-β1 was upregulated at weeks 6 and 8 upon liver fibrosis induction. During tTG inhibition, TGF-β1 level decreased in sera and liver of infected mice. TGF-β1 showed positive staining in liver containing Sj adult worms and eggs. TGF-β1 was also detected in Sj adult worm sections, soluble egg antigen and Sj adult worm antigen, and adult worms' culture medium. The TGF-β1 mature peptide cDNA sequence and its extended sequence were amplified through RT-PCR and RACE-PCR using adult worms as template, and sequence is analyzed and loaded to NCBI GenBank (number GQ338152.1). TGF-β1 transcript in Sj eggs was higher than in adult worms. In Sj-infected liver, transcriptional level of TGF-β1 from Sj, but not mouse liver, correlated with liver fibrosis extent. This study provides evidence that tTG regulates TGF-β1 and illustrates the importance of targeting tTG in treating Sj infection-induced fibrosis.
Highlights
Schistosomiasis is one of the nine neglected tropical diseases that received much attention over the last several years
We investigated the association between Tissue transglutaminase (tTG) and TGF-β1 that originated from the host or from Schistosoma japonicum (Sj) using Sj-infected mice as liver fibrosis model
We previously reported a high extent of post-Sj-infection hepatic fibrosis in mice
Summary
Schistosomiasis is one of the nine neglected tropical diseases that received much attention over the last several years. The portal blood flow carries the eggs into the liver where they induce production of inflammatory granuloma and, subsequently, tissue repair and fibrosis. Schistosoma japonicum (Sj) mainly damages mammalian hosts by producing liver granuloma and fibrosis [1]. Transforming growth factor (TGF-β1) is one of the strongest factors that lead to liver fibrosis. The relationship between TGF-β1, liver fibrosis, and Schistosoma infection is controversial. TGF-β1 has sometimes been accepted as the key factor inducing liver granuloma and fibrosis during Sj infection because some researchers have recognized TGF-β1 inhibition as one of Mediators of Inflammation the factors that can be used to evaluate the antifibrotic effects of drugs on hosts infected with Sj [9,10,11]. Systemic studies that reveal whether liver fibrosis caused by Sj infection is dependent or not dependent on TGF-β1 are lacking
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