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POQI-10 Infographics

Fig. 1 The gastrointestinal epithelium in health and disease. A A healthy intestinal barrier consists of intestinal epithelial cells that are constantly renewed through maturation and migration of multipotent crypt progenitors, and intact junctions that hold epithelial cells in tight apposition. In contrast, epithelial cell damage, decreased proliferation, and apoptosis combine with failed intercellular junctions to compromise intestinal barrier integrity and allow bacterial translocation. B The submucosal plexis supplies blood to the gut mucosa. The arrangement of the arterioles and venules allows for countercurrent exchange of oxygen. Created with BioRender.com
Fig. 1 The gastrointestinal epithelium in health and disease. A A healthy intestinal barrier consists of intestinal epithelial cells that are constantly renewed through maturation and migration of multipotent crypt progenitors, and intact junctions that hold epithelial cells in tight apposition. In contrast, epithelial cell damage, decreased proliferation, and apoptosis combine with failed intercellular junctions to compromise intestinal barrier integrity and allow bacterial translocation. B The submucosal plexis supplies blood to the gut mucosa. The arrangement of the arterioles and venules allows for countercurrent exchange of oxygen. Created with BioRender.com


Fig. 2 Distribution of blood fow in critical illness. During stress states, such as those found in critical illness, blood fow is redistributed away from the gut to favor perfusion of the heart, brain, and lungs. Created with BioRender.com
Fig. 2 Distribution of blood fow in critical illness. During stress states, such as those found in critical illness, blood fow is redistributed away from the gut to favor perfusion of the heart, brain, and lungs. Created with BioRender.com


Fig. 3 Consequences of GI barrier failure. Injury to the GI tract can occur from intraluminal and extraluminal sources. Regardless of the source of injury, intestinal epithelial cells and innate and adaptive immune cells in the lamina propria release chemical messages (cytokines, chemokines, and DAMPs) that act locally and travel through the blood and lymph, resulting in infammation throughout the GI system and the entire body. The numbers in this fgure correspond to the potential therapeutic targets, found in Table 2. DAMP, damage-associated molecular pattern; MAMP, microbe-associated molecular pattern; PMN, polymorphonuclear leukocytes; PRR, pattern recognition receptor.
Fig. 3 Consequences of GI barrier failure. Injury to the GI tract can occur from intraluminal and extraluminal sources. Regardless of the source of injury, intestinal epithelial cells and innate and adaptive immune cells in the lamina propria release chemical messages (cytokines, chemokines, and DAMPs) that act locally and travel through the blood and lymph, resulting in infammation throughout the GI system and the entire body. The numbers in this fgure correspond to the potential therapeutic targets, found in Table 2. DAMP, damage-associated molecular pattern; MAMP, microbe-associated molecular pattern; PMN, polymorphonuclear leukocytes; PRR, pattern recognition receptor.


Fig. 4 TLR signaling activated by GI failure. TLR are responsible for detection of microbial components that cross the gut mucosal barrier into host tissues. The best characterized of the TLR is TLR4, which senses LPS from Gram negative bacteria. IL-1, interleukin; IFN, interferon; IRAK, IL-1 receptor associated kinase; IRF3, interferon regulatory factor 3; LPS, lipopolysaccharide; MyD88, myeloid diferentiation factor 88; NF-κB, nuclear factor kappa B; MAP3K7, mitogen-activated protein kinase kinase 7 (also known as TAK1); TIR, toll/interleukin-1 receptor; TLR, toll like receptor; TNFa, tumor necrosis factor alphal; TICAM1, Toll-IL-1 receptor domain-containing adaptor molecule (also known as TRIF).
Fig. 4 TLR signaling activated by GI failure. TLR are responsible for detection of microbial components that cross the gut mucosal barrier into host tissues. The best characterized of the TLR is TLR4, which senses LPS from Gram negative bacteria. IL-1, interleukin; IFN, interferon; IRAK, IL-1 receptor associated kinase; IRF3, interferon regulatory factor 3; LPS, lipopolysaccharide; MyD88, myeloid diferentiation factor 88; NF-κB, nuclear factor kappa B; MAP3K7, mitogen-activated protein kinase kinase 7 (also known as TAK1); TIR, toll/interleukin-1 receptor; TLR, toll like receptor; TNFa, tumor necrosis factor alphal; TICAM1, Toll-IL-1 receptor domain-containing adaptor molecule (also known as TRIF).


Fig. 5 Susceptibility to endotoxemia and downstream systemic efects. A Humans are much more sensitive to LPS than most other species. B Endotoxemia results in systemic sequelae, impacting numerous organ systems and may result in multi-organ dysfunction. LPS, lipopolysaccharide.
Fig. 5 Susceptibility to endotoxemia and downstream systemic efects. A Humans are much more sensitive to LPS than most other species. B Endotoxemia results in systemic sequelae, impacting numerous organ systems and may result in multi-organ dysfunction. LPS, lipopolysaccharide.