Related Mechanisms of Secondary Infections in Hepatic Cirrhosis Patients

Abstract

Context: End-stage liver disease (ESLD), the terminal phase of chronic hepatic disorders, is characterized by profound liver dysfunction and heightened susceptibility to secondary infections. Cirrhosis, a key manifestation of ESLD, impairs innate and adaptive immunity via structural and functional hepatic abnormalities. Evidence Acquisition: A detailed literature review was conducted to synthesize recent advances in understanding the immunological mechanisms underlying the increased infection risk in cirrhotic patients, focusing on Kupffer cell dysfunction, complement system deficiencies, elevated Pro-inflammatory cytokines, and impaired T-cell responses. Results: Dysfunctional Kupffer cells exhibit impaired pathogen clearance, while defects in the complement system compromise opsonization and phagocytosis. Elevated levels of Interleukin-2 (IL-2) disrupt the differentiation of T follicular helper (Tfh) cells, impairing antibody production and further compromising adaptive immunity. Concurrently, aberrant expression of HLA-DR and dysregulation of immune checkpoints reflect systemic immune exhaustion. Conclusions: Collectively, these mechanisms increase susceptibility to infections and sepsis, highlighting the critical interplay between innate and adaptive immune dysfunctions in compromising the body's ability to effectively respond to pathogens.