Next Article in Journal
Deprotonation Mechanism of Methyl Gallate: UV Spectroscopic and Computational Studies
Next Article in Special Issue
The Role of Adipokines in Surgical Procedures Requiring Both Liver Regeneration and Vascular Occlusion
Previous Article in Journal
Systemic Platelet-Activating Factor-Receptor Agonism Enhances Non-Melanoma Skin Cancer Growth
Previous Article in Special Issue
Danger-Associated Molecular Patterns (DAMPs): Molecular Triggers for Sterile Inflammation in the Liver
Article Menu
Issue 10 (October) cover image

Export Article

Open AccessReview
Int. J. Mol. Sci. 2018, 19(10), 3110; https://doi.org/10.3390/ijms19103110

CEACAM1 in Liver Injury, Metabolic and Immune Regulation

1
Institute of Experimental Immunology and Hepatology, Center for Experimental Medicine, University Medical Center Hamburg-Eppendorf, Martinistraße 52, 20251 Hamburg, Germany
2
Department of Biomedical Sciences, Heritage College of Osteopathic Medicine, Irvine Hall, 1 Ohio University, Athens, OH 45701-2979, USA
3
The Diabetes Institute, Heritage College of Osteopathic Medicine, Irvine Hall, 1 Ohio University, Athens, OH 45701-2979, USA
4
University Medical Center Hamburg-Eppendorf, Martinistraße 52, 20251 Hamburg, Germany
These authors contributed equally to this article.
*
Author to whom correspondence should be addressed.
Received: 31 August 2018 / Revised: 2 October 2018 / Accepted: 4 October 2018 / Published: 11 October 2018
(This article belongs to the Special Issue Liver Damage and Repair)
Full-Text   |   PDF [2271 KB, uploaded 11 October 2018]   |  

Abstract

Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is a transmembrane glycoprotein that is expressed on epithelial, endothelial and immune cells. CEACAM1 is a differentiation antigen involved in the maintenance of epithelial polarity that is induced during hepatocyte differentiation and liver regeneration. CEACAM1 regulates insulin sensitivity by promoting hepatic insulin clearance, and controls liver tolerance and mucosal immunity. Obese insulin-resistant humans with non-alcoholic fatty liver disease manifest loss of hepatic CEACAM1. In mice, deletion or functional inactivation of CEACAM1 impairs insulin clearance and compromises metabolic homeostasis which initiates the development of obesity and hepatic steatosis and fibrosis with other features of non-alcoholic steatohepatitis, and adipogenesis in white adipose depot. This is followed by inflammation and endothelial and cardiovascular dysfunctions. In obstructive and inflammatory liver diseases, soluble CEACAM1 is shed into human bile where it can serve as an indicator of liver disease. On immune cells, CEACAM1 acts as an immune checkpoint regulator, and deletion of Ceacam1 gene in mice causes exacerbation of inflammation and hyperactivation of myeloid cells and lymphocytes. Hence, hepatic CEACAM1 resides at the central hub of immune and metabolic homeostasis in both humans and mice. This review focuses on the regulatory role of CEACAM1 in liver and biliary tract architecture in health and disease, and on its metabolic role and function as an immune checkpoint regulator of hepatic inflammation. View Full-Text
Keywords: CEACAM1; immune checkpoint receptor; liver disease; insulin clearance CEACAM1; immune checkpoint receptor; liver disease; insulin clearance
Figures

Graphical abstract

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
SciFeed

Share & Cite This Article

MDPI and ACS Style

Horst, A.K.; Najjar, S.M.; Wagener, C.; Tiegs, G. CEACAM1 in Liver Injury, Metabolic and Immune Regulation. Int. J. Mol. Sci. 2018, 19, 3110.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top