BACKGROUND: Chronic hepatitis B (HBV) and hepatitis C (HCV) patients have elevated plasma levels of soluble CD14 (sCD14). We examined whether human hepatocytes produce sCD14 in vivo, and whether HBV or HCV infections influence this chimeric production. METHODS: uPA-SCID mice were transplanted with primary human hepatocytes and some animals were subsequently infected with HBV or HCV. Plasma from these mice was analyzed for the presence of human sCD14. The liver was examined via immunohistochemistry. RESULTS: A soluble form of human CD14 could be detected in the plasma from successfully transplanted mice, while it was completely absent in non-transplanted control animals. The isoform of this human sCD14 corresponded with the most abundant isoform found in human plasma. CD14 levels in circulation were not significantly different between non-infected, HBV infected and HCV infected animals. CONCLUSIONS: Our data indicate that human hepatocytes produce sCD14 in vivo, and that liver cells might be the major source of sCD14 in normal human plasma. In addition we demonstrate that HBV and HCV infections have no direct influence on the production of sCD14 by human hepatocytes in this chimeric model.
BACKGROUND:Chronic hepatitis B (HBV) and hepatitis C (HCV) patients have elevated plasma levels of soluble CD14 (sCD14). We examined whether human hepatocytes produce sCD14 in vivo, and whether HBV or HCV infections influence this chimeric production. METHODS:uPA-SCID mice were transplanted with primary human hepatocytes and some animals were subsequently infected with HBV or HCV. Plasma from these mice was analyzed for the presence of human sCD14. The liver was examined via immunohistochemistry. RESULTS: A soluble form of humanCD14 could be detected in the plasma from successfully transplanted mice, while it was completely absent in non-transplanted control animals. The isoform of this human sCD14 corresponded with the most abundant isoform found in human plasma. CD14 levels in circulation were not significantly different between non-infected, HBV infected and HCV infected animals. CONCLUSIONS: Our data indicate that human hepatocytes produce sCD14 in vivo, and that liver cells might be the major source of sCD14 in normal human plasma. In addition we demonstrate that HBV and HCV infections have no direct influence on the production of sCD14 by human hepatocytes in this chimeric model.
Authors: M Bethel; P Bůžková; H A Fink; J A Robbins; J A Cauley; J Lee; J I Barzilay; D I Jalal; L D Carbone Journal: Osteoporos Int Date: 2015-12-11 Impact factor: 4.507
Authors: Tamara Timmons; Changyu Shen; Grace Aldrovandi; Adrienne Rollie; Samir K Gupta; James H Stein; Michael P Dubé Journal: AIDS Res Hum Retroviruses Date: 2013-10-08 Impact factor: 2.205
Authors: Robert C Kaplan; Alan L Landay; Howard N Hodis; Stephen J Gange; Philip J Norris; Mary Young; Kathryn Anastos; Phyllis C Tien; Xiaonan Xue; Jason Lazar; Christina M Parrinello; Lorie Benning; Russell P Tracy Journal: J Acquir Immune Defic Syndr Date: 2012-08-01 Impact factor: 3.731