Up-Regulation of Intestinal Toll-Like Receptors and Cytokines Expressions Change After TPN Administration and a Lack of Enteral Feeding

Ikeda, Takuto; Hiromatsu, Kenji; Hotokezaka, Masayuki; Chijiiwa, Kazuo

doi:10.1016/j.jss.2009.01.022

Cited by 19 publications

(17 citation statements)

References 25 publications

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“…32 Furthermore, TPN administration in mice has been shown to result in increased TLR expression in the gut leading to hyper-response to bacterially derived ligands 33 . We employed the intestinal loop model to delineate the impact of suppression of endogenous IAP on luminal pro-inflammatory molecules during enteral starvation.…”

Section: Resultsmentioning

confidence: 99%

“…38 Furthermore, a lack of enteral feeding increases intestinal inflammation and results in an increased sensitivity to luminal pro-inflammatory mediators. 32, 33 Miyasaka et al showed that the blockade of Myd88, a downstream signaling molecule of TLRs, prevents intestinal inflammation and barrier dysfunction seen in a mouse TPN model. 15 Similarly, inhibition of TNF-α signaling was shown to ameliorate the impairment in intestinal permeability due to enteral starvation.…”

Section: Discussionmentioning

confidence: 99%

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A Novel Approach to Maintain Gut Mucosal Integrity Using an Oral Enzyme Supplement

et al. 2014

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Objective To determine the role of intestinal alkaline phosphatase (IAP) in enteral starvation-induced gut barrier dysfunction and to study its therapeutic effect as a supplement to prevent gut-derived sepsis. Background Critically ill patients are at increased risk for systemic sepsis and, in some cases, multi-organ failure leading to death. Years ago, the gut was identified as a major source for this systemic sepsis syndrome. Previously, we have shown that IAP detoxifies bacterial toxins, prevents endotoxemia, and preserves intestinal microbiotal homeostasis. Methods WT and IAP- KO mice were used to examine gut barrier function and tight junction protein levels during 48 h starvation and fed states. Human ileal fluid samples were collected from 20 patients post ileostomy and IAP levels were compared between fasted and fed states. To study the effect of IAP supplementation on starvation-induced gut barrier dysfunction, WT mice were fasted for 48 h +/− IAP supplementation in the drinking water. Results The loss of IAP expression is associated with decreased expression of intestinal junctional proteins and impaired barrier function. For the first time, we demonstrate that IAP expression is also decreased in humans who are deprived of enteral feeding. Finally, our data demonstrates that IAP supplementation reverses the gut barrier dysfunction and tight junction protein losses due to a lack of enteral feeding. Conclusions IAP is a major regulator of gut mucosal permeability and is able to ameliorate starvation-induced gut barrier dysfunction. Enteral IAP supplementation may represent a novel approach to maintain bowel integrity in critically-ill patients.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

A Novel Approach to Maintain Gut Mucosal Integrity Using an Oral Enzyme Supplement

et al. 2014

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“…In the literature, TPN has been shown to be a risk factor for systemic infections in patients [13–15]. Animal studies indicate that TPN predisposes to a hyperactive response to infection [8,9,16]. The findings of our study suggest that TPN and/or gut disuse may prime the body for a hyperactive inflammatory response in a more general sense than just to infection as in this case the response to a different type of stress, intestinal surgery.…”

Section: Discussionmentioning

confidence: 99%

“…Animal studies have shown that TPN and lack of enteral nutrition cause local increased gut inflammation and breakdown of gut barrier function which can increase bacterial translocation [9–11,16]. Obstruction and intestinal infection also affect the intestinal microbiome [17].…”

Section: Discussionmentioning

confidence: 99%

Profound systemic inflammatory response syndrome following non-emergent intestinal surgery in children

Chawla

Teitelbaum

2013

Journal of Pediatric Surgery

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Purpose Systemic inflammatory response syndrome (SIRS) is an uncommon but severe complication in surgical patients. While SIRS is well known, it is poorly described in the pediatric population. The goal of this study was to describe the incidence of profound SIRS following non-emergent intestinal surgery in children and to identify potential risk factors. Methods A retrospective review was conducted for patients 0–19 years of age following intestinal surgery and/or lysis of adhesions from 01/01/1999-02/28/2012. Children were excluded for preoperative instability or frank bowel perforation. Patients were then placed in a post-operative SIRS or non-SIRS group as defined by the 2005 International Pediatric Sepsis Consensus Conference Guidelines (6. B. Goldstein, B. Giroir, A. Randolph, and Sepsis International Consensus Conference on Pediatric, ‘International Pediatric Sepsis Consensus Conference: Definitions for Sepsis and Organ Dysfunction in Pediatrics’, Pediatr Crit Care Med, 6 (2005), 2–8.). Results SIRS was identified in 17 of the 381 patients. Logistic regression analysis was performed and showed heart disease, kidney disease, PN dependence, and intestinal obstruction to be predictive of post-operative SIRS. Conclusion This study represents one of the first reports to identify a previously poorly described process of significant SIRS after intestinal surgery in children. Both systemic organ failure and intestinal dysfunction are strong risk factors for post-operative SIRS in children. Potentially, these pre-existing conditions may lead to disruption of normal intestinal flora or barrier function, which in turn may predispose these children for dramatic SIRS after intestinal surgery. Understanding how these factors lead to SIRS will be critical to developing prevention strategies.

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“…From the clinical point of view, gastroparesis and impaired colonic motility represent a major problem in critically ill patients, since enteral nutrition is often not sufficiently possible, leading to reflux, aspiration, and bacterial translocation as a consequence of impaired passage in the large bowel [4,5].…”

Section: Introductionmentioning

confidence: 99%

The Gut is not only the Target but a Source of Inflammatory Mediators Inhibiting Gastrointestinal Motility During Sepsis

Königsrainer¹,

Türck²,

Eisner³

et al. 2011

Cell Physiol Biochem

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Background: Sepsis is a common problem in intensive care patients leading to multi-organ failure and gastrointestinal paralysis. Aim: The aim of the study was to investigate whether the gastrointestinal tract is not only the target but also the source of inflammatory mediators inhibiting gastrointestinal motility. Methods: Mesenteric lymph was obtained from rats in which a sepsis was induced by lipopolysaccharide (LPS) intraperitoneally. Gastrointestinal motility was recorded following mesenteric lymph- or TNFα infusion into the jugular vein of separate healthy recipient rats using the strain gauge transducer technique. Results: Infusion of sepsis lymph significantly impairs gastric and colonic motility, decreasing the motility-index in the stomach and colon by about 57% and 21% respectively in comparison to baseline motility. Among other inflammatory mediators, TNFα plays an important role in mediating the inhibitory effect of mesenteric lymph on gastrointestinal motility during sepsis. Conclusions: The gastrointestinal tract is the source and the target of inflammatory mediators released during sepsis causing paralytic ileus.

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Up-Regulation of Intestinal Toll-Like Receptors and Cytokines Expressions Change After TPN Administration and a Lack of Enteral Feeding

Cited by 19 publications

References 25 publications

A Novel Approach to Maintain Gut Mucosal Integrity Using an Oral Enzyme Supplement

A Novel Approach to Maintain Gut Mucosal Integrity Using an Oral Enzyme Supplement

Profound systemic inflammatory response syndrome following non-emergent intestinal surgery in children

The Gut is not only the Target but a Source of Inflammatory Mediators Inhibiting Gastrointestinal Motility During Sepsis

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