somuch4food
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Immunity and Gastrointestinal Disease: A Role for Lymphatic Vessels
Below are some interesting quotes from the article. I invite others to read it though because I still do not have enough knowledge to fully grasp it.
"There is also a strong link between the lymphatic system and bacterial translocation, in which passage of viable bacteria occurs from the intestinal lumen into the mucosa and muscle layer to extra-intestinal sites. These instances can be promoted by bacterial overgrowth in the intestine, host immune deficiencies and in situations of increased permeability of the intestinal wall such as inflammatory bowel diseases „
"The lymphatic system, like most tissues in the body, responds to inflammatory mediators during an acute or chronic inflammatory response. One of the hallmark effects of inflammatory mediators is to stimulate vascular leakage, which increases interstitial fluid volumes. "
"Furthermore, studies have shown that nitric oxide, a vasoactive molecule implicated in the inflammatory response, also limits lymphatic contractile activity [19,23]. Histamine, an inflammatory mediator that is crucial for increasing microvascular permeability has also been shown to have a direct stimulatory effect on lymphatic contractility and function [24-26]. This potent effect of histamine on lymphatic function has implications on the pathogenesis of food allergies, as large amounts of histamine are released during mast-cell degranulation. This has been shown to increase lymphatic contraction frequency [27]. Other inflammatory mediators, such as serotonin and as well as neuropeptides, have impacts on lymphatic contractility [19] but are beyond the scope of this review. „
"While the lymphatic system is clearly pivotal for immunity and fluid homeostasis in the entire body, it is even more closely linked with the gastrointestinal system because of its role in nutrient absorption and immune cell trafficking to this area. The relationship between the gut and the lymphatic system has also been shown to be critical during intestinal inflammation. IBD patients presenting with oedema were reported to have enlarged lymphatic vessels, which appeared obstructed [37-40]. The enlarged and stenotic lymphatic vessels suggest poor lymphatic drainage, which would further exacerbate the tissue oedema. Interestingly, animal studies where mesenteric lymphatic drainage was experimentally obliterated led to Crohn’s disease-like macroscopic and microscopic patterns [40-42]. These animal models of lymphatic obstruction are considered by some to best reproduce Crohn’s disease symptoms without contribution from genes, environment or bacterial makeup in the gut [31]. Importantly, these animal models of lymphatic obstruction recapitulate transmural inflammation and intestinal fistulae characteristic of Crohn’s disease [42]. "
"A study reporting that a large number of DC and proliferating T cells were found in the lamina propria of Crohn’s disease patients, suggests that they are unable to be drained away by the lymphatic system and are trapped at the site of inflammation forming lymphoid aggregates, and creating a self-perpetuating feedback loop that prolongs the local immune response [48]."
Below are some interesting quotes from the article. I invite others to read it though because I still do not have enough knowledge to fully grasp it.
"There is also a strong link between the lymphatic system and bacterial translocation, in which passage of viable bacteria occurs from the intestinal lumen into the mucosa and muscle layer to extra-intestinal sites. These instances can be promoted by bacterial overgrowth in the intestine, host immune deficiencies and in situations of increased permeability of the intestinal wall such as inflammatory bowel diseases „
"The lymphatic system, like most tissues in the body, responds to inflammatory mediators during an acute or chronic inflammatory response. One of the hallmark effects of inflammatory mediators is to stimulate vascular leakage, which increases interstitial fluid volumes. "
"Furthermore, studies have shown that nitric oxide, a vasoactive molecule implicated in the inflammatory response, also limits lymphatic contractile activity [19,23]. Histamine, an inflammatory mediator that is crucial for increasing microvascular permeability has also been shown to have a direct stimulatory effect on lymphatic contractility and function [24-26]. This potent effect of histamine on lymphatic function has implications on the pathogenesis of food allergies, as large amounts of histamine are released during mast-cell degranulation. This has been shown to increase lymphatic contraction frequency [27]. Other inflammatory mediators, such as serotonin and as well as neuropeptides, have impacts on lymphatic contractility [19] but are beyond the scope of this review. „
"While the lymphatic system is clearly pivotal for immunity and fluid homeostasis in the entire body, it is even more closely linked with the gastrointestinal system because of its role in nutrient absorption and immune cell trafficking to this area. The relationship between the gut and the lymphatic system has also been shown to be critical during intestinal inflammation. IBD patients presenting with oedema were reported to have enlarged lymphatic vessels, which appeared obstructed [37-40]. The enlarged and stenotic lymphatic vessels suggest poor lymphatic drainage, which would further exacerbate the tissue oedema. Interestingly, animal studies where mesenteric lymphatic drainage was experimentally obliterated led to Crohn’s disease-like macroscopic and microscopic patterns [40-42]. These animal models of lymphatic obstruction are considered by some to best reproduce Crohn’s disease symptoms without contribution from genes, environment or bacterial makeup in the gut [31]. Importantly, these animal models of lymphatic obstruction recapitulate transmural inflammation and intestinal fistulae characteristic of Crohn’s disease [42]. "
"A study reporting that a large number of DC and proliferating T cells were found in the lamina propria of Crohn’s disease patients, suggests that they are unable to be drained away by the lymphatic system and are trapped at the site of inflammation forming lymphoid aggregates, and creating a self-perpetuating feedback loop that prolongs the local immune response [48]."
