Abstract

Postinjury multiple organ failure results from an inappropriate overwhelming immune response to injury. During trauma and hemorrhagic shock (T/HS), mesenteric ischemia causes gut mucosal breakdown with disruption of the intestinal barrier. It has been proposed that this releases the gut microbiota systemically via postshock mesenteric lymph (PSML), engendering infectious complications. Despite extensive investigation, no clear evidence has been presented for gut bacterial translocation after resuscitation from T/HS. However, such previous studies were limited by available technologies. More sensitive methods, such as quantitative polymerase chain reaction, have since emerged for detection of bacterial presence and danger-associated molecular patterns (DAMPs). Quantitative polymerase chain reaction was applied to PSML derived from a rat model of T/HS. No bacterial presence was detected in a series of 12 samples, whereas multiple lymph samples showed the presence of DAMPs after T/HS. Thus, we confirmed that bacterial translocation does not exist in PSML after resuscitation from T/HS-associated mesenteric ischemia. However, T/HS does increase the presence of mitochondrial DAMPs in PSML. These results support our current position that PSML elaborates remote organ injury by multiple inflammatory mechanisms, including lipid-mediated proinflammatory stimuli, and by contribution from gut-derived DAMPs.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.