Circulating lipocalin 2 is neither related to liver steatosis in patients with non-alcoholic fatty liver disease nor to residual liver function in cirrhosis

Meier, Elisabeth M.; Pohl, Rebekka; Rein-Fischboeck, Lisa; Schacherer, Doris; Eisinger, Kristina; Wiest, Reiner; Krautbauer, Sabrina; Buechler, Christa

doi:10.1016/j.cyto.2016.06.004

Cited by 10 publications

(7 citation statements)

References 37 publications

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“…Furthermore, human serum LCN2 is a biomarker of acute-on-chronic liver failure and prognosis in cirrhosis 16 and reported to correlate to non-alcoholic fatty liver disease (NAFLD) 17 , ASH disease severity, and the model for end-stage liver disease (MELD) score 18 . We and others did not find systemic LCN2 levels to directly correlate to impaired liver function and disease severity 15 , 19 . We here used the 8 week-repeated carbon tetrachloride (CCl 4 ) intraperitoneal injections of female C57BL/6 wild type and Lcn2 −/− mice to evaluate the role of LCN2 in hepatic inflammation and fibrosis.…”

Section: Introductioncontrasting

confidence: 60%

Chronic mineral oil administration increases hepatic inflammation in wild type mice compared to lipocalin 2 null mice

Borkham-Kamphorst

Haas

Pinoé-Schmidt

et al. 2021

Laboratory Investigation

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Lipocalin 2 (LCN2), an acute-phase protein produced during acute liver injury, plays an important role in the innate immune response against bacterial infection via iron scavenging. LCN2 further influences neutrophil development and physiology leading to increased inflammatory responses. We investigated the roles of LCN2 in chronic inflammation and fibrosis, using repeated carbon tetrachloride (CCl4) in mineral-oil injection. Surprisingly, mice treated with the mineral oil vehicle alone showed liver inflammation, evidenced by neutrophil and monocyte-macrophage infiltration. Fluorescence-activated cell sorting (FACS) of isolated liver leukocytes showed significantly high CD45+ leukocyte concentrations in CCl4 mice, but no difference of Ly6G+ neutrophils between mineral oil and CCl4 application. Liver CD11b+ F4/80+ cells counted higher in CCl4 mice, but the proportions of Gr1high, an indicator of inflammation, were significantly higher in mineral oil groups. Liver myeloperoxidase (MPO), expressed in neutrophils and monocytes, showed higher levels in wild type mice compared to Lcn2−/− in both mineral-oil and CCl4 treated groups. Hepatic and serum LCN2 levels were remarkably higher in the mineral oil-injected wild type group compared to the CCl4. Wild type animals receiving mineral oil showed significantly higher inflammatory cytokine- and chemokine mRNA levels compared to Lcn2−/− mice, with no differences in the CCl4 treated groups. RNA sequencing (RNA-Seq) confirmed significant downregulation of gene sets involved in myeloid cell activation and immune responses in Lcn2 null mice receiving chronic mineral oil versus wild−type. We observed significant upregulation of gene sets and proteins involved in cell cycle DNA replication, with downregulation of collagen-containing extracellular matrix genes in Lcn2–/– mice receiving CCl4, compared to the wild type. Consequently, the wild type mice developed slightly more liver fibrosis compared to Lcn2−/− mice, evidenced by higher levels of collagen type I in the CCl4 groups and no liver fibrosis in mineral oil-treated mice. Our findings indicate that serum and hepatic LCN2 levels correlate with hepatic inflammation rather than fibrosis.

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Section: Introductioncontrasting

confidence: 60%

Chronic mineral oil administration increases hepatic inflammation in wild type mice compared to lipocalin 2 null mice

Borkham-Kamphorst

Haas

Pinoé-Schmidt

et al. 2021

Laboratory Investigation

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“…Adipocytes produce LCN2 in response to pro-inflammatory cytokine exposure (22, 23, 24) and several immune cell types also produce LCN2 (25). However, substantial evidence indicates that circulating LCN2 is liver–derived and produced in response to infection or injury (26, 27), so it is not surprising that the changes we observed in LCN2 levels in this study were only at the level of the eWAT itself and not in serum (Figure 4B). The role of LCN2 in adipose tissue is generally thought to be pro-inflammatory, since increasing its expression promotes neutrophil recruitment and induces pro-inflammatory cytokine production (28, 29), although anti-inflammatory effects have been reported in other tissues (30, 31).…”

Section: Discussionmentioning

confidence: 63%

Adipose Tissue Dysfunction Occurs Independently of Obesity in Adipocyte‐Specific Oncostatin Receptor Knockout Mice

Stephens

Bailey

Hang

et al. 2018

Obesity

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“…This cohort has been recently described . Of the 148 patients examined, 56 were suitable for this study (Fig.…”

Section: Methodsmentioning

confidence: 99%

Hepatic chemerin mRNA expression is reduced in human nonalcoholic steatohepatitis

Pohl

Haberl

Rein-Fischboeck

et al. 2016

Eur J Clin Investigation

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Circulating lipocalin 2 is neither related to liver steatosis in patients with non-alcoholic fatty liver disease nor to residual liver function in cirrhosis

Cited by 10 publications

References 37 publications

Chronic mineral oil administration increases hepatic inflammation in wild type mice compared to lipocalin 2 null mice

Chronic mineral oil administration increases hepatic inflammation in wild type mice compared to lipocalin 2 null mice

Adipose Tissue Dysfunction Occurs Independently of Obesity in Adipocyte‐Specific Oncostatin Receptor Knockout Mice

Hepatic chemerin mRNA expression is reduced in human nonalcoholic steatohepatitis

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