| First Author | Li ZY | Year | 2019 |
| Journal | Parasit Vectors | Volume | 12 |
| Issue | 1 | Pages | 302 |
| PubMed ID | 31200771 | Mgi Jnum | J:289892 |
| Mgi Id | MGI:6435085 | Doi | 10.1186/s13071-019-3542-4 |
| Citation | Li ZY, et al. (2019) Contribution of tissue transglutaminase to the severity of hepatic fibrosis resulting from Schistosoma japonicum infection through the regulation of IL-33/ST2 expression. Parasit Vectors 12(1):302 |
| abstractText | BACKGROUND: Tissue transglutaminase (tTG)-regulating IL-13 plays an important role in the pathogenesis of liver fibrosis resulting from Schistosoma japonicum (Sj) infection. IL-33 and its receptor ST2 are involved in Th2-biased immune responses through the release of IL-5 and IL-13 and subsequent hepatic granuloma pathology induced by Sj infection. However, the relationship between tTG, IL-33/ST2, and liver fibrosis during Schistosoma infection has not been established. RESULTS: This study investigated the link between tTG and IL-33/ST2 in the induction of liver fibrogenesis during Sj infection in mice. The extent of liver fibrosis coincided with an increase in tTG and IL-33/ST2 expression in the liver of infected mice between five to eight weeks, with a peak of correlation at six weeks after Sj infection. The inhibition of tTG activity through cystamine administration or gene knockout alleviated the level of TLR4, NF-kappaB pathway molecules, IL-33/ST2, and the severity of liver fibrosis resulting from Sj infection. CONCLUSIONS: These results indicate that during Sj infection tTG may control liver fibrosis at least partially through TLR4, NF-kappaB pathway activation and then IL-33/ST2. tTG, IL-33 or ST2 might be promising drug targets against liver fibrosis induced by Sj infection. |
