The intestinal microbiota and the function and structure of the GI tract are altered by changes brought on by critical illness.

In the setting of increasing oxidative stress, where the pH or P O 2PO2 levels within the lumen of the gut may drop, pathogenic bacteria like Pseudomonas and staphylococci undergo quorum sensing

If the number of organisms is high enough, these pathogenic bacteria express virulent genes, which allows adherence to the intestinal surface and a contact-dependent activation of the intestinal epithelial cell. A cytokine storm results with the release of inflammatory agents (interleukin-1, interleukin-8, and tumor necrosis factor) into lymphatic channels. A gut-lung conduit of inflammation results, as these cytokines pass through lymphatic channels and mesenteric lymph nodes into the thoracic duct and ultimately into the systemic circulation via the left subclavian vein. These proinflammatory cytokines pass directly into the microcapillary system of the lungs where activation of platelet activating factor and neutrophils lead to acute respiratory distress syndrome.