Elevated TGF-beta1 levels might protect HCV/ HIV-coinfected patients from liver fibrosis

2011 European Journal of Clinical Investigation 41;1 (70-76)

BACKGROUND: HIV accelerates hepatitis C virus (HCV)-induced liver fibrosis by mechanisms not well understood. As HIV dysregulates transforming growth factor-beta1 (TGF-beta1) 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-beta1 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-beta1 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-beta1 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-beta1 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-beta1, probably through its anti-inflammatory effects, might protect HCV/HIV-coinfected patients from liver fibrosis.

Pubmed : 20868448