Exploring the mechanism and potential treatment of severe acute pancreatitis-associated lung injury based on the gut-lung axis

Abstract

Severe acute pancreatitis (SAP), a prevalent and life-threatening abdominal emergency, is characterized by its abrupt onset, rapid progression, and high mortality rate, frequently precipitating multiple organ dysfunction syndromes. Acute lung injury (ALI) represents the most common early complication of SAP. ALI may progress to acute respiratory distress syndrome, which constitutes the primary cause of mortality in patients with SAP. However, the precise pathogenesis underlying ALI in SAP remains incompletely elucidated. Notably, recent advances in gut-lung axis research have significantly advanced our understanding of SAP-associated ALI (SAP-ALI). The gut-lung axis, a sophisticated bidirectional communication network linking the intestines and lungs, facilitates crosstalk between the microbiota and their metabolites across both organs via lymphatic and circulatory systems alongside the mucosal immune system. Critically, research confirms that SAP induces severe gut microbiota dysbiosis. This dysbiosis disrupts the intestinal mucosal barrier, enabling bacterial and endotoxin translocation to the lungs through lymphatic and hematogenous routes. Concurrently, gut-derived immune cells migrate to the lungs via the bloodstream, directly contributing to pulmonary immune-inflammatory imbalance. Consequently, this review synthesized the central role of the gut-lung axis in SAP-ALI pathogenesis and explored emerging therapeutic strategies targeting this pivotal axis, aiming to provide novel insights for the clinical prevention and treatment of SAP-ALI.

Keywords: Severe acute pancreatitis-associated acute lung injury; Gut-lung axis; Intestinal microbiota; Bacterial translocation; Migration of immune cells

Core Tip: Severe acute pancreatitis (SAP)-associated acute lung injury is a pivotal determinant of mortality. The gut-lung axis plays a central role in its pathogenesis. SAP-induced gut microbiota dysbiosis compromises the intestinal barrier, facilitating bacterial/endotoxin translocation and gut-derived immune cell migration to the lungs. This process culminates in a profound pulmonary inflammatory response, thereby identifying the gut-lung axis as a promising therapeutic target for novel interventions against SAP-associated acute lung injury.