Abstract
Gut-derived infection is among the most common complications in patients who underwent severe trauma, serious burn, major surgery, hemorrhagic shock or severe acute pancreatitis (SAP). It could cause sepsis and multiple organ dysfunction syndrome (MODS), which are regarded as a leading cause of mortality in these cases. Gut-derived infection is commonly caused by pathological translocation of intestinal bacteria or endotoxins, resulting from the dysfunction of the gut barrier. In the last decades, the studies regarding to the pathogenesis of gut-derived infection mainly focused on the breakdown of intestinal epithelial tight junction and increased permeability. Limited information is available on the roles of intestinal microbial barrier in the development of gut-derived infection. Recently, advances of next-generation DNA sequencing techniques and its utilization has revolutionized the gut microecology, leading to novel views into the composition of the intestinal microbiota and its connections with multiple diseases. Here, we reviewed the recent progress in the research field of intestinal barrier disruption and gut-derived infection, mainly through the perspectives of the dysbiosis of intestinal microbiota and its interaction with intestinal mucosal immune cells. This review presents novel insights into how the gut microbiota collaborates with mucosal immune cells to involve the development of pathological bacterial translocation. The data might have important implication to better understand the mechanism underlying pathological bacterial translocation, contributing us to develop new strategies for prevention and treatment of gut-derived sepsis.
Highlights
Bacterial infections are common complications in critically ill patients, likely leading to sepsis, multiple organ dysfunction, and even death [1]
The gut may serve as the motor of multiple organ dysfunction syndromes (MODS), probably derived from intestinal bacterial translocation and subsequent acute septic responses [4, 5]
Bacterial translocation is defined as the process in which the intestinal bacteria and/or their products spread through the gut barrier into the extra-intestinal sites, including the mesenteric lymph nodes (MLNs), systemic circulation, and distant organs [25, 26]
Summary
Bacterial infections are common complications in critically ill patients, likely leading to sepsis, multiple organ dysfunction, and even death [1]. The gut may serve as the motor of multiple organ dysfunction syndromes (MODS), probably derived from intestinal bacterial translocation and subsequent acute septic responses [4, 5]. The gut microbiota has a key role in maintaining the gut homeostasis by establishing and maintaining beneficial interaction with mucosal immune cells and intestinal epithelial cells [23] In critical illness, this interaction could become pathological due to alterations of the gut microbiota, leading to the loss of intestinal homeostasis, bacterial translocation, gut-derived sepsis, and deleterious clinical sequelaes [24]. We discussed how the gut microbiota drives bacterial translocation through alterations in microbial community architecture, modulation of innate and adaptive immunity, and disruption of the mucosal barrier in critical illness. We discussed the therapeutic potential to modify the intestinal microbiota with fecal microbiota transplantation (FMT)
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