Fig. 2

Liver damage contributes to the development of acute respiratory distress syndrome. Liver injury leads to changes in the expression of acute-phase proteins (APPs) and to an increase in plasma levels of bacteria/bacterial products, pro-inflammatory cytokines, and pro-coagulant and vasoactive factors in the lung and systemic circulation. These mediators generate deleterious effects on the lung (passage of bacteria /bacterial products and inflammation) and on the gut (intestinal dysbiosis, impairment of gut barrier integrity, leakage of bacteria/bacterial products into the portal circulation and into the mesenteric lymph), resulting in relevant changes in the hepatic and pulmonary microbiota and promoting inflammation and oxidative stress in liver and lung tissues. In addition, lung-derived cytokines promote the synthesis of APPs and activation of inflammatory responses in the liver. All these responses mediated by the gut–liver–lung axis contribute to lung injury and multiple organ dysfunction in critical illness. IL interleukin, TNF tumor necrosis factor, INF interferon