BACKGROUND: HIV accelerates hepatitis C virus (HCV)-induced liver fibrosis by mechanisms not well understood. As HIV dysregulates transforming growth factor-β1 (TGF-β1) and T regulatory (Treg) cells, both of which are involved in hepatic fibrogenesis, herein we describe their influence on liver fibrosis staging in patients with chronic hepatitis C with and without HIV coinfection. METHODS: Eighty-eight subjects (42 HIV/HCV co-infected patients, 20 HCV-monoinfected patients, and 26 healthy controls) were examined. Treg cells (CD4+Foxp3+) were measured in peripheral blood using flow cytometry. An enzyme immunoassay was used to measure TGF-β1 in plasma. Liver fibrosis staging was estimated using elastometry and advanced liver fibrosis was considered for ≥ 9·5 kPa (F3-F4 Metavir estimates). RESULTS: Treg cells were increased in HIV/HCV-coinfected patients compared with HCV-monoinfected patients (P = 0·004), whereas TGF-β1 levels were similar in both groups of patients. While Treg cells levels were similar in both null-mild and advanced liver fibrosis patients, a high level of TGF-β1 was found in patients with low levels of liver fibrosis compared with those with advanced liver fibrosis [14·9 ng mL(-1) (5·6-37·9) vs. 5·5 ng mL(-1) (1·9-7·9) respectively P = 0·007]. In a multivariate logistic regression model, elevated TGF-β1 levels were significantly associated with not having advanced liver fibrosis [OR: 0·13 (95% CI: 0·02-0·71), P = 0·019]. CONCLUSIONS: While Treg cells do not influence liver fibrosis staging, elevated TGF-β1, probably through its anti-inflammatory effects, might protect HCV/HIV-coinfected patients from liver fibrosis.
BACKGROUND: HIV accelerates hepatitis C virus (HCV)-induced liver fibrosis by mechanisms not well understood. As HIV dysregulates transforming growth factor-β1 (TGF-β1) and T regulatory (Treg) cells, both of which are involved in hepatic fibrogenesis, herein we describe their influence on liver fibrosis staging in patients with chronic hepatitis C with and without HIV coinfection. METHODS: Eighty-eight subjects (42 HIV/HCV co-infectedpatients, 20 HCV-monoinfected patients, and 26 healthy controls) were examined. Treg cells (CD4+Foxp3+) were measured in peripheral blood using flow cytometry. An enzyme immunoassay was used to measure TGF-β1 in plasma. Liver fibrosis staging was estimated using elastometry and advanced liver fibrosis was considered for ≥ 9·5 kPa (F3-F4 Metavir estimates). RESULTS: Treg cells were increased in HIV/HCV-coinfectedpatients compared with HCV-monoinfected patients (P = 0·004), whereas TGF-β1 levels were similar in both groups of patients. While Treg cells levels were similar in both null-mild and advanced liver fibrosispatients, a high level of TGF-β1 was found in patients with low levels of liver fibrosis compared with those with advanced liver fibrosis [14·9 ng mL(-1) (5·6-37·9) vs. 5·5 ng mL(-1) (1·9-7·9) respectively P = 0·007]. In a multivariate logistic regression model, elevated TGF-β1 levels were significantly associated with not having advanced liver fibrosis [OR: 0·13 (95% CI: 0·02-0·71), P = 0·019]. CONCLUSIONS: While Treg cells do not influence liver fibrosis staging, elevated TGF-β1, probably through its anti-inflammatory effects, might protect HCV/HIV-coinfectedpatients from liver fibrosis.
Authors: Shaoyong Li; Lianne E M Vriend; Imad A Nasser; Yury Popov; Nezam H Afdhal; Margaret J Koziel; Detlef Schuppan; Mark A Exley; Nadia Alatrakchi Journal: Hepatology Date: 2012-12 Impact factor: 17.425
Authors: Pamela Valva; Paola Casciato; Juan M Diaz Carrasco; Adrian Gadano; Omar Galdame; María Cristina Galoppo; Eduardo Mullen; Elena De Matteo; María Victoria Preciado Journal: PLoS One Date: 2011-08-17 Impact factor: 3.240
Authors: Pilar Garcia-Broncano; Luz Maria Medrano; Juan Berenguer; Juan González-García; Mª Ángeles Jiménez-Sousa; Ana Carrero; Victor Hontañón; Josep M Guardiola; Manuel Crespo; Carmen Quereda; José Sanz; Ana Belen García-Gómez; Jose Luis Jimenez; Salvador Resino Journal: Cells Date: 2018-11-02 Impact factor: 6.600