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Abstract
The intestinal community, including the commensal microbial flora as well as the host tissues, represents a functional whole in vivo. Under physiological circumstances, this symbiosis brings great benefit for the host; however, critical illness induces profound disturbances in the intestinal ecosystem affecting both procaryotic and eucaryotic members. Today, 25 years after the gut was first described as a motor of multiple organ dysfunction syndrome, the role of the injured splanchnic compartment in the pathomechanism and development of critical illness is still in the first line of research. Multiple mechanisms have been identified by which the stressed gut may affect host homeostasis, and how external intervention might help to rebalance physiology. This paper provides a brief overview of the present of this field.
Highlights
The gastrointestinal system represents an enormous surface to the internal world of the gut microbiome and nutrient antigens
Faced with the enormous amount of bacteria and nutrient antigens, the mucosal immune network consists of the intestinal epithelium, intraepithelial lymphocytes, and the immune apparatus of the lamina propria, Peyer’s patches, and mesenteric lymph nodes
The original theory was based on the conception that bacteria translocating to the circulation through the injured intestinal barrier in critical illness facilitate systemic inflammatory responses and contribute to the development of multiple organ dysfunction syndrome (MODS). This model was supported by the fact that germ-free animals improved survival after hemorrhagic shock/intestinal ischemia-reperfusion compared to controls [40, 41]
Summary
The gastrointestinal system represents an enormous surface to the internal world of the gut microbiome and nutrient antigens. Faced with the enormous amount of bacteria and nutrient antigens, the mucosal immune network consists of the intestinal epithelium, intraepithelial lymphocytes, and the immune apparatus of the lamina propria, Peyer’s patches, and mesenteric lymph nodes. Intestinal dendritic cells, which are able to hold live commensal bacteria for several days, are as well retained to a well-determined niche via mesenteric lymph nodes, that function as a filter for these cells as shown by a mouse model [14] This way, the mucosal immune responses are kept partially separated from the systemic compartment, allowing local IgA production but avoiding inadequate immunization with enteral bacteria and potential consequent enterocolitis or autoimmune complications.
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