Bacterial translocation increases phagocytic activity of polymorphonuclear leucocytes in portal hypertension: priming independent of liver cirrhosis

Neugebauer, Hermann; Hartmann, Pia; Krenn, Sebastian; Glück, Thomas; Schölmerich, Jürgen; Straub, Rainer H.; Wiest, Reiner

doi:10.1111/j.1478-3231.2008.01829.x

Cited by 29 publications

(31 citation statements)

References 40 publications

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“…Multiple studies have documented a number of pro-and anti-inflammatory markers in the serum and ascitic fluid of such patients [17,18] . Furthermore, an immune response, both innate and adaptive, can be generated and exacerbated by a network of immunocytes sampling bacterial antigens in the enteric mucosa or after BT [29][30][31][32][33][34][35][36][37] . These processes are in a dynamic equilibrium, wherein a particular arrangement of inflammatory markers, both in the serum and ascitic fluid, interacts with a critical load of bacterial antigen.…”

Section: Discussionmentioning

confidence: 99%

“…Its significance in measuring ascitic fluid inflammation and/or infection, e.g., SBP, is less well characterized [28] . It has been shown that many of these same cytokines are generated by activated macrophages, neutrophils, NK cells and lymphocytes in peri-peritoneal tissues in cirrhotic patients [29][30][31][32][33][34] . These immune cells are activated upon sensing appropriate bacterial antigens, such as bacterial DNA or lipopolysaccharide, either in the intestinal mucosa or after BT.…”

Section: Introductionmentioning

confidence: 99%

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

Attar

Moore

George

et al. 2014

WJG

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Attar

Moore

George

et al. 2014

WJG

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“…Cirrhotic rats are characterized by bacterial translocation. 17,23 Interestingly, the intraperitoneal application of bacterial endotoxin affected portal pressure and enhanced the response to the microbial constituents that reached the liver through the portal vein. Different routes of bacterial constituents into the portal vein as a 'second hit' are conceivable.…”

Section: Effects Of Lps Pretreatment On Portal Pressurementioning

confidence: 99%

“…17,18 In this study, the effects of intraperitoneal LPS on portal pressure and the involved pathways were investigated.…”

mentioning

confidence: 99%

Intraperitoneal LPS amplifies portal hypertension in rat liver fibrosis

Steib¹,

Hartmann²,

Hesler³

et al. 2010

Laboratory Investigation

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Recent studies have shown that the risk of variceal bleeding in patients with liver cirrhosis increases with infections such as spontaneous bacterial peritonitis (SBP). In this study, we hypothesized that pretreatment with intraperitoneal LPS may escalate portal hypertension. In fibrotic livers (4 weeks after bile duct ligation, BDL), the activation of Kupffer cells (KCs) by zymosan (150 mg/ml) in the isolated non-recirculating liver perfusion system resulted in a transient increase in portal perfusion pressure. Pretreatment with intraperitoneal LPS (1 mg/kg body weight (b.w.) for 3 h) increased basal portal perfusion pressure, and prolonged the zymosan-induced increase from transient to a long-lasting increase that was sustained until the end of the experiments in BDL but not in sham-operated animals. Pretreatment with gadolinium chloride (10 mg/kg b.w.), MK-886 (0.6 mg/kg b.w.), Ly171883 (20 mM) or BM 13.177 (20 mM) reduced the maximal and long-lasting pressure increase in BDL animals by approximately 50-60%. The change in portal perfusion pressure was paralleled by a long-lasting production of cysteinyl leukotriene (Cys-LT) and thromboxane (TX) after LPS pretreatment. However, the response to vasoconstrictors was not altered by intraperitoneal LPS. Western blot analyses showed an increased Toll-like receptor (TLR)4 and MyD88 expression after LPS pretreatment. In vivo experiments confirmed that intraperitoneal LPS increased basal portal pressure, and extended the portal pressure increase produced by intraportal zymosan or by LPS infusion. In conclusion, upregulation of TLR4 and MyD88 expression in fibrotic livers confers hypersensitivity to LPS. This may lead to escalation of portal hypertension by production of TX and Cys-LT after endotoxin-induced KC activation. Therefore, LT inhibitors may represent a promising treatment option in addition to early administration of antibiotics in SBP.

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“…Several authors examined a significant role of intestinal endotoxemia and bacterial translocation in the pathogenesis of HPS [72][73][74][75]. Endotoxins are lipopolysaccharides and components of inner monolayer of Gram-negative bacterial membrane [76].…”

Section: Intestinal Endotoxemiamentioning

confidence: 99%