| First Author | Cao S | Year | 2020 |
| Journal | Biochem Biophys Res Commun | Volume | 525 |
| Issue | 3 | Pages | 654-661 |
| PubMed ID | 32122655 | Mgi Jnum | J:297872 |
| Mgi Id | MGI:6479355 | Doi | 10.1016/j.bbrc.2020.02.139 |
| Citation | Cao S, et al. (2020) Helicobacter hepaticus infection-induced IL-33 promotes hepatic inflammation and fibrosis through ST2 signaling pathways in BALB/c mice. Biochem Biophys Res Commun 525(3):654-661 |
| abstractText | It has been documented that Helicobacter hepaticus (H. hepaticus) infection is linked to hepatic inflammation and fibrosis. Interleukin 33 (IL-33) is a cytokine involved in inflammatory and fibrotic diseases, but its relevance to H. hepaticus infection-induced liver inflammation and fibrosis is unknown. In this study, we found that the expression of IL-33 in mice liver was significantly induced by H. hepaticus infection at 24 weeks post infection (WPI). Immunohistochemistry analysis revealed that IL-33 was transferred from the nucleus to the cytoplasm due to infection. The quantitation of inflammatory cytokine and histopathology evaluation showed that IL-33 knockdown attenuated the H. hepaticus-induced hepatic inflammation and fibrosis. More importantly, H. hepaticus promoted the expression of the IL-33 receptor ST2 on cell surfaces, and the expression of ST2 then activated the expression nuclear factor-kappaB (p65), alpha-SMA, and Erk1/2. These observations provide novel insights into the pathogenic mechanism of hepatic inflammation and fibrosis during H. hepaticus infection. |
