Elevated TGF-β1 levels might protect HCV/HIV-coinfected patients from liver fibrosis
Elevated TGF-β1 levels might protect HCV/HIV-coinfected patients from liver fibrosis
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DOI：
10.1111/j.1365-2362.2010.02381.x
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发表时间：
2011-01-01
影响因子：
5.5
通讯作者：
Benito, Jose M.
中科院分区：
文献类型：
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作者：
Rallon, Norma I.;Barreiro, Pablo;Benito, Jose M.
P>背景HIV 加速丙型肝炎病毒 (HCV) 诱导的肝纤维化，其机制尚不清楚。由于 HIV 失调转化生长因子-β 1 (TGF-β 1) 和调节性 T (Treg) 细胞，这两种细胞都参与肝纤维化，因此我们在本文中描述了它们对合并或不合并 HIV 感染的慢性丙型肝炎患者肝纤维化分期的影响。 方法 对 88 名受试者（42 名 HIV/HCV 合并感染患者、20 名 HCV 单感染患者和 26 名健康对照）进行了检查。使用流式细胞术测量外周血中的 Treg 细胞 (CD4+Foxp3+)。使用酶免疫测定法测量血浆中的TGF-β1。使用弹性测量法估计肝纤维化分期，≥9中心点5 kPa（F3-F4 Metavir估计）被认为是晚期肝纤维化。结果与HCV单一感染患者相比，HIV/HCV合并感染患者的Treg细胞增加（P = 0中心点004），而两组患者的TGF-β1水平相似。虽然轻度肝纤维化患者和晚期肝纤维化患者的 Treg 细胞水平相似，但与晚期肝纤维化患者相比，肝纤维化水平较低的患者中 TGF-β1 水平较高[分别为 14 中心点 9 ng mL-1（5 中心点 6-37 中心点 9）与 5 中心点 5 ng mL-1（1 中心点 9-7 中心点 9），P = 0 中心点007]。在多变量 Logistic 回归模型中，TGF-β 1 水平升高与未发生晚期肝纤维化显着相关 [OR：0 中心点 13（95% CI：0 中心点 02-0 中心点 71），P = 0 中心点 019]。结论 虽然 Treg 细胞不影响肝纤维化分期，但 TGF-β 1 水平升高可能通过其抗炎作用，可能保护肝纤维化。 HCV/HIV 合并感染的肝纤维化患者。
P>BackgroundHIV accelerates hepatitis C virus (HCV)-induced liver fibrosis by mechanisms not well understood. As HIV dysregulates transforming growth factor-beta 1 (TGF-beta 1) 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.MethodsEighty-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-beta 1 in plasma. Liver fibrosis staging was estimated using elastometry and advanced liver fibrosis was considered for >= 9 center dot 5 kPa (F3-F4 Metavir estimates).ResultsTreg cells were increased in HIV/HCV-coinfected patients compared with HCV-monoinfected patients (P = 0 center dot 004), whereas TGF-beta 1 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-beta 1 was found in patients with low levels of liver fibrosis compared with those with advanced liver fibrosis [14 center dot 9 ng mL-1 (5 center dot 6-37 center dot 9) vs. 5 center dot 5 ng mL-1 (1 center dot 9-7 center dot 9) respectively P = 0 center dot 007]. In a multivariate logistic regression model, elevated TGF-beta 1 levels were significantly associated with not having advanced liver fibrosis [OR: 0 center dot 13 (95% CI: 0 center dot 02-0 center dot 71), P = 0 center dot 019].ConclusionsWhile Treg cells do not influence liver fibrosis staging, elevated TGF-beta 1, probably through its anti-inflammatory effects, might protect HCV/HIV-coinfected patients from liver fibrosis.