Peritoneal immunity in decompensated cirrhosis

In patients with cirrhosis and ascites, failure of intestinal barriers and cirrhosis-associated immune dysfunction contribute to the translocation of bacteria and microbial products to the peritoneal cavity, which promotes infection, perpetuates inflammation and accelerates acute-on-chronic liver failure. Resident peritoneal immune cells are repeatedly exposed to bacterial products and their activation status is linked to complications of spontaneous bacterial peritonitis. This narrative review summarizes the recent research on human peritoneal immunity in decompensated cirrhosis focusing on the altered composition and functional states of human peritoneal macrophages, resident and migrating T cells, and neutrophils and their involvement in peritoneal inflammation and infection. Peritoneal immune cells in decompensated cirrhosis show compartmentalized chronic activation and dysfunction, contributing to inflammation and infection risk. Given the direct accessibility of these cells, targeting peritoneal macrophage priming and differentiation, innate immune memory, inflammatory mediators and intercellular peritoneal cross-talk offer potential strategies to prevent infections and mitigate inflammation. To fine-tune the delicate balance between hyperinflammation and anergy, further research is necessary to translate immunomodulatory approaches into effective clinical interventions.