Causes and Consequences of Innate Immune Dysfunction in Cirrhosis
- 1Mater Research Institute, University of Queensland, Australia
- 2Princess Alexandra Hospital, Australia
- 3Faculty of Medicine, The University of Queensland, Australia
Liver cirrhosis is an increasing health burden and public health concern. Regardless of etiology, patients with cirrhosis are at risk of a range of life-threatening complications, including the development of infections, which are associated with high morbidity and mortality and frequent hospital admissions. The term Cirrhosis-Associated Immune Dysfunction (CAID) refers to a dynamic spectrum of immunological perturbations that develop in patients with cirrhosis, which are intimately linked to the underlying liver disease, and negatively correlated with prognosis. At the two extremes of the CAID spectrum are systemic inflammation, which can exacerbate clinical manifestations of cirrhosis such as hemodynamic derangement and kidney injury; and immunodeficiency, which contributes to the high rate of infection in patients with decompensated cirrhosis. Innate immune cells, in particular monocytes/macrophages and neutrophils, are pivotal effector and target cells in CAID. This review focuses on the pathophysiological mechanisms leading to impaired innate immune function in cirrhosis. Knowledge of the phenotypic manifestation and pathophysiological mechanisms of cirrhosis associated immunosuppression may lead to immune targeted therapies to reduce susceptibility to infection in patients with cirrhosis, and better biomarkers for risk stratification and assessment of efficacy of novel immunotherapies.
Keywords: Innate immnuity, Decompensated chirrosis, Infection, monocyte, Ascites
Received: 27 Sep 2018;
Accepted: 05 Feb 2019.
Edited by:Reiner Wiest, University Children’s Hospital Bern, Switzerland
Reviewed by:Dan A. Mitchell, University of Warwick, United Kingdom
Joan Clària, Hospital Clínic de Barcelona, Spain
Copyright: © 2019 Irvine, Ratnasekera, Powell and Hume. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Dr. Katharine M. Irvine, Mater Research Institute, University of Queensland, Brisbane, Australia, email@example.com