Abstract
Acute-on-chronic liver failure (ACLF) is a complex syndrome that develops in patients with acutely decompensated cirrhosis. In this condition, dysbalanced immune function and excessive systemic inflammation are closely associated with organ failure and high short-term mortality. In this review, we describe how omic technologies have contributed to the characterization of the hyperinflammatory state in patients with acutely decompensated cirrhosis developing ACLF, with special emphasis on the role of metabolomics, lipidomics and transcriptomics in profiling the triggers (pathogen- and damage-associated molecular patterns [PAMPs and DAMPs]) and effector molecules (cytokines, chemokines, growth factors and bioactive lipid mediators) that lead to activation of the innate immune system. This review also describes how omic approaches can be invaluable tools to accelerate the identification of novel biomarkers that could guide the implementation of novel therapies/interventions aimed at protecting these patients from excessive systemic inflammation and organ failure.
Highlights
Acute-on-chronic liver failure (ACLF) is a complex syndrome that develops in patients with acutely decompensated cirrhosis
We describe how omic technologies have contributed to the characterization of the hyperinflammatory state in patients with acutely decompensated cirrhosis developing ACLF, with special emphasis on the role of metabolomics, lipidomics and transcriptomics in profiling the triggers and effector molecules that lead to activation of the innate immune system
This review describes how omic approaches can be invaluable tools to accelerate the identification of novel biomarkers that could guide the implementation of novel therapies/interventions aimed at protecting these patients from excessive systemic inflammation and organ failure
Summary
ACLF is a severe syndrome resulting in high short-term mortality evolving in patients with acutely decompensated (AD) liver cirrhosis. Recent advances in understanding the pathophysiology of ACLF have identified an association between systemic inflammation and organ injury in patients with AD cirrhosis developing ACLF [4,5,6] This systemic hyperinflammatory state is produced by the massive release of inflammatory mediators such as cytokines, chemokines, growth factors and bioactive lipid mediators with potential to induce immune-mediated tissue damage, a process known as immunopathology. Systemic inflammation can occur in patients with AD cirrhosis and ACLF in the absence of bacterial infections and/or bacterial translocation as the result of the release of damage-associated molecular patterns (DAMPs) from injured organs and tissues (Figure 1). Components of the innate immune system into account, the overall immune status in patients with ACLF ranges within the spectrum from immunosuppressive/immunoregulatory/tolerogenic to vigorously hyperinflammatory, and these extremes are not mutually exclusive
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