1. Corrigendum to “Lipocalin-2 mediates non-alcoholic steatohepatitis by promoting neutrophil-macrophage crosstalk via the induction of CXCR2” 
Dewei Ye, Kangmin Yang, Shufei Zang, Zhuofeng Lin, Hau-Tak Chau, Yudong Wang, Jialiang Zhang, Junping Shi, Aimin Xu, Shaoqiang Lin, Yu Wang 
Journal of Hepatology 
Volume 66, Issue 3, (March 2017)
DOI: /j.jhep
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2. Fig. 6
Mice lacking CXCR2 are resistant to lipocalin-2-evoked liver inflammation and injury. Four-week-old male CXCR2 knockout (KO) and wild-type (WT) littermates were fed with either standard chow (SC) or high fat high cholesterol (HFHC) diet for 20weeks. During the last 4weeks, mice were subjected to continuous infusion of recombinant mouse LCN2 protein (rm-LCN2) using osmotic pumps as in Fig. 4. (A) Representative images of H&E staining in liver sections (left, scale bar, 10μm) and semi-quantification for histological lesions in left panel. (B, C) Representative images of liver sections immunostained for F4/80 (B, left; scale bar, 10μm) and Ly6G (C, left; scale bar, 10μm) and quantification for the numbers of F4/80-positive (B, right) and Ly6G-positive (C, left) cells per 400× microscope field. Hepatic mRNA expression levels of CXCR2 and CXCL2 (D), together with proinflammatory cytokines (TNF-α and IL-1β) and chemokine (MCP-1) (E), were determined by quantitative real time PCR. Data are expressed as mean±SEM, n=5–6. ∗p<0.05; ∗∗p<0.01. (This figure appears in colour on the web.)
Journal of Hepatology  , DOI: ( /j.jhep )
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