Lcn2 levels in PV after CCl4 treatment were significantly decreas

Lcn2 levels in PV after CCl4 treatment were significantly decreased in SPX mice compared to Sham mice (327.5 ± 35.0 ng/mL vs 465.9 ± 30.6 ng/mL, p<0.05). CCL2 and TNF-α mRNA levels were significantly decreased after rLcn2 treatment on LPS-stimulated KCs. Conclusion: Spleen

deficiency enhanced CCl4-induced liver fibrosis. The mechanism of exaggerated liver fibrosis most likely involves decreased Lcn2 levels in PV that led to excessive KC activation in this check details model. The spleen may have a protective role in the development of liver fibrosis by Lcn2 produced from Gr1-positive cells, and it could be a new therapeutic target against liver fibrosis. Disclosures: The following people have nothing to disclose: Tomonori Aoyama, Akira Uchiyama, Kazuyoshi Kon, Hironao

Okubo, Shunhei Yamashina, Kenichi Ikejima, Shigehiro Kokubu, Akihisa Miyazaki, Sumio Watanabe Introduction: Lysyl Oxidase Like 2 (LOXL2) is an extracellular copper-dependent amine oxidase that catalyzes the formation of crosslinks in collagen. We assessed the relationship of sLOXL2 levels with liver fibrosis and cirrhosis in patients with CHB treated with TDF. Methods: Subjects in the pivotal TDF registration trials who had stored serum samples available for analysis at baseline and weeks 12, 48 and 240 were included in the analysis. Liver biopsies were selleck chemicals performed pre-treatment, at weeks 48 and 240. sLOXL2 was measured using a highly sensitive assay developed using 2 specific monoclonal antibodies on a Singulex® platform. Results: Of the 641 selleck compound subjects originally randomized, 304 had stored serum available and were included in the analysis. Of these, 225 had liver biopsies at baseline and week 240. Characteristics (77% male, 63% white, 30% Asian and 13% obese) of the subjects included in the study matched well with those not included

in the analysis. sLOXL2 correlated with Ishak fibrosis stage at all time points. In cross sectional analyses at baseline, the median sLOXL2 level correlated with necroinflammation by Knodell score (p<0.0001) and with fibrosis by Ishak stage (791 pg/mL for Ishak stage 0-2, 1091 pg/mL for Ishak 3-4 and 1370 for pg/mL for Ishak 5-6; p<0.0001). In longitudinal analysis, sLOXL2 declined with treatment, with the largest decline seen in the first 12 weeks. For all fibrosis stage categories, patients experiencing fibrosis regression consistently had lower sLOXL2 levels than those without regression (Figure1). Conclusions: sLOXL2 correlates with fibrosis stage in patients with HBV. sLOXL2 declines with HBV treatment, likely indicating a decrease in fibrogenesis. Overall, the data suggest that sLOXL2 is a potential measure of ongoing fibrosing disease and may be useful not only to assess liver fibrosis at a given time but also to detect reversal of fibrosis and cirrhosis. Mean Serum L0XL2 (+/- SE) by Baseline Ishak Fibrosis Score, Stratified by Regression Status Disclosures: W.

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