kangaSue
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Looking into the function of the mesentery after the recent interest in the media that this is now being considered as a new organ, there was something of interest in a paper that caught my attention.
The digestive tract as the origin of systemic inflammation;
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5067918/
[Many of these infections are initiated by translocation of intestinal bacteria and usually result in bacteremia and, in more severe cases, sepsis [42]. Bacterial translocation can be demonstrated by analysis of mesenteric lymphatics or portal vein blood samples. It is important to point out here that, in a classic study, portal vein sampling in trauma patients undergoing laparotomy did not provide evidence for bacterial translocation by blood cultures [43]. Subsequent studies with trauma patients confirmed that blood cultures generally failed to show bacterial growth [44, 45]. However, more sensitive methods, such as immunostaining for E. coli beta-galactosidase [44] or electron microscopy [45], provided direct evidence for bacterial translocation to mesenteric lymph nodes (MLNs) in most patients. While the presence of bacteria in MLNs as a pathological event has been debated [46, 47], multiple studies have shown that positive cultures from MLN samples obtained from laparotomy patients occurred in 10–15 % of patients, which correlated with an increased risk of postoperative sepsis [48, 49] or postoperative infection [50].]
For the most part, research into this is only from the aspect of being critically ill and or post-injury or post-operative infection but I saw it mentioned in a paper by Maes that it also occurs in those with ME/CFS so it would be no surprise if it's found to happen in lesser manifestations of chronic illness involving gut dysfunction too.
http://bmcmedicine.biomedcentral.com/articles/10.1186/1741-7015-11-64
Increased bacterial translocation is also associated with the onset of ME/CFS [199]. Loosening of the gut barrier may allow poorly invasive Gram-negative bacteria to translocate from the gut into the mesenteric lymph nodes and sometimes into the blood stream. Once translocated, the LPS is recognized by the Toll-like receptor 4 (TLR4) complex, which primes immune cells and consequently activates inflammatory and Oxidative & Nitrosative Stress pathways [12, 199].
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4575624/
A "clean case" of systemic injury; Mesenteric lymph after hemorrhagic shock elicits a sterile inflammatory response.
[Post-injury 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 post-shock mesenteric lymph, engendering infectious complications.]
Anyone got any ideas on how this could be stopped from happening?
The digestive tract as the origin of systemic inflammation;
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5067918/
[Many of these infections are initiated by translocation of intestinal bacteria and usually result in bacteremia and, in more severe cases, sepsis [42]. Bacterial translocation can be demonstrated by analysis of mesenteric lymphatics or portal vein blood samples. It is important to point out here that, in a classic study, portal vein sampling in trauma patients undergoing laparotomy did not provide evidence for bacterial translocation by blood cultures [43]. Subsequent studies with trauma patients confirmed that blood cultures generally failed to show bacterial growth [44, 45]. However, more sensitive methods, such as immunostaining for E. coli beta-galactosidase [44] or electron microscopy [45], provided direct evidence for bacterial translocation to mesenteric lymph nodes (MLNs) in most patients. While the presence of bacteria in MLNs as a pathological event has been debated [46, 47], multiple studies have shown that positive cultures from MLN samples obtained from laparotomy patients occurred in 10–15 % of patients, which correlated with an increased risk of postoperative sepsis [48, 49] or postoperative infection [50].]
For the most part, research into this is only from the aspect of being critically ill and or post-injury or post-operative infection but I saw it mentioned in a paper by Maes that it also occurs in those with ME/CFS so it would be no surprise if it's found to happen in lesser manifestations of chronic illness involving gut dysfunction too.
http://bmcmedicine.biomedcentral.com/articles/10.1186/1741-7015-11-64
Increased bacterial translocation is also associated with the onset of ME/CFS [199]. Loosening of the gut barrier may allow poorly invasive Gram-negative bacteria to translocate from the gut into the mesenteric lymph nodes and sometimes into the blood stream. Once translocated, the LPS is recognized by the Toll-like receptor 4 (TLR4) complex, which primes immune cells and consequently activates inflammatory and Oxidative & Nitrosative Stress pathways [12, 199].
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4575624/
A "clean case" of systemic injury; Mesenteric lymph after hemorrhagic shock elicits a sterile inflammatory response.
[Post-injury 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 post-shock mesenteric lymph, engendering infectious complications.]
Anyone got any ideas on how this could be stopped from happening?