Bacterial Translocation to Mesenteric Lymph Nodes Increases in Chronic Portal Hypertensive Rats

Abstract

The enlargement of the stenosed portal tract related to triple partial portal vein ligation in the rat, since it increases the resistance to the portal blood flow, may be a key factor involved in one of the pathological consequences of portal hypertension, as is bacterial translocation to mesenteric lymph nodes.

Procalcitonin, and cytokines document a dynamic inflammatory state in non-infected cirrhotic patients with ascites

“…Other noncellular inflammatory markers in SBP have been studied as well, including ascitic fluid lactoferrin, with productive results [37,38] . Interestingly though, even in non-infected cirrhotic patients with portal hypertensive ascites, there seems to be a significant degree of cellular and cytokine inflammation [16][17][18] . Multiple studies have documented a number of pro-and anti-inflammatory markers in the serum and ascitic fluid of such patients [17,18] .…”

“…Consistent with these facts, it known that oral medications such as cisapride and trimethoprim-sulfamethoxazole can attenuate bacterial overgrowth, enhance mucosal function, and increase intestinal transit, all leading to reduced rates of BT [13][14][15] . Even in the absence of overt infection, there is a significant inflammatory response in cirrhotic patients occurring as a result of a complex interaction of pro-and anti-inflammatory cytokines consisting of numerous interleukins, tumor necrosis factor-alpha (TNF-α), interferon gamma (IFNγ) and complement proteins [16][17][18] . This concerted cytokine response has both temporal and site specific properties in cirrhotic patients with portal hypertension [16,17] .…”

“…Even in the absence of overt infection, there is a significant inflammatory response in cirrhotic patients occurring as a result of a complex interaction of pro-and anti-inflammatory cytokines consisting of numerous interleukins, tumor necrosis factor-alpha (TNF-α), interferon gamma (IFNγ) and complement proteins [16][17][18] . This concerted cytokine response has both temporal and site specific properties in cirrhotic patients with portal hypertension [16,17] . One particular inflammatory marker is procalcitonin (PCT), a 116 amino acid protein made in multiple sites of the body including liver and intestine.…”

Portal hypertension-related inflammatory phenotypes: From a vitelline and amniotic point of view

“…The expression of the immune phenotype by the splanchnic system which has suffered ischemia and/or reperfusion is coupled with interstitial infiltration by inflammatory cells and by bacteria [30][31][32]. It has been hypothesized that the symbiosis of inflammatory cells and bacteria for extracellular (fermentation) and intracellular (phagocytosis) could favor tissue trophism [2,10].…”

“…Likewise, the natural inhibitors of matrix metalloproteinases (TIMPs) could promote anti-enzymatic stress [3]. Portal hypertension is one factor determining bacterial intestinal translocation to mesenteric lymph nodes [30,32]. In addition, the increased presence of mast cells in the hypertrophied mesenteric lymph nodes of prehepatic portal hypertensive rats [35,36] would not only collaborate in the production of mesenteric adenitis, but also it would constitute a source of inflammatory mediators located between the intestine and systemic blood circulation [37,38].…”