Clinical significance of translocation.

Leeuwen, Paul A. M. van; Boermeester, M. A.; Houdijk, Alexander P. J.; Ferwerda, Charlotte C.; C, Ma; Meyer, S.; Wesdorp, R. I. C.

doi:10.1136/gut.35.1_suppl.s28

Cited by 262 publications

(137 citation statements)

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“…The onset of sepsis usually occurs following an excessive or uncontrolled inflammatory response (18). The causal relationship between intestinal damage and sepsis indicates that the intestinal tract is not only a target organ, but also the starting point of sepsis (5,19). The LPS endotoxin is one of the most notable components of the bacterial cell wall, and is released into the host during bacterial growth, reproduction, lysis, or cell death (3).…”

Section: Discussionmentioning

confidence: 99%

Rhein inhibits lipopolysaccharide-induced intestinal injury during sepsis by blocking the toll-like receptor 4 nuclear factor-κB pathway

Zhang

Jiao

et al. 2015

Molecular Medicine Reports

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Abstract. Sepsis is one of the leading causes of mortality in severe systemic inflammatory syndrome. The endotoxin-induced inflammatory response has been linked to the development of sepsis. Rhein is a lipophilic anthraquinone isolated from Rheum rhabarbarum (rhubarb), which has a protective effect on intestinal damage in vivo. However, the underlying mechanism responsible for the protective effects of rhein remains to be elucidated. In the present study, mice were exposed to 20 mg/kg lipopolysaccharide (LPS), prior to being treated with either 100 mg/kg rhein or 0.3 mg/kg toll-like receptor 4 (TLR4) signaling inhibitor TAK-242. In the rhein-treated mice, the colon length (cm) was extended and colon injury was attenuated. In addition, treatment with rhein significantly decreased the expression levels of the LPS-induced inflammatory cytokines interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-α, in both the plasma and colon tissue. However, mice treated with TAK-242 exhibited increased expression levels of IL-10, as determined by ELISA and western blot analysis. In addition, immunohistochemistry and western blot analyses demonstrated that treatment with rhein was able to reduce TLR4 expression and inhibit nuclear factor-κB (NF-κB) phosphorylation in colon tissue. Furthermore, LPS induction was blocked by TAK-242. These results demonstrate that the observed rhein-attenuated inflammatory response during sepsis may be achieved via the TLR4 NF-κB signaling pathway. In conclusion, the results of the present study provide a novel insight into the protective effects of rhein on LPS-induced intestinal inflammation, and demonstrate that rhein may act as a beneficial therapeutic agent in the treatment of sepsis-induced intestinal damage.

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Section: Discussionmentioning

confidence: 99%

Rhein inhibits lipopolysaccharide-induced intestinal injury during sepsis by blocking the toll-like receptor 4 nuclear factor-κB pathway

Zhang

Jiao

et al. 2015

Molecular Medicine Reports

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“…49 Endotoxin can be transported through the lymphatic channels, bypass the liver or enter the peritoneal cavity directly and can cause systemic endotoxaemia. 50 Endotoxin can also increase intestinal permeability directly 51 or by stimulating primed macrophages to release an excessive amount of cytokines, mostly TNF-␣, thereby inducing mucosal inflammation and increasing permeability. 52 Higher levels of circulating endotoxin are obtained after giving intensive TBI containing regimens 13 suggesting that persistent low-grade endotoxaemia or the inflammation associated with MBI induce fever of unknown origin since endotoxaemia and gut mucosal damage occurred in 44 (70%) of 63 HSC transplant recipients (both allogeneic and autologous) all of whom developed fever that could not be explained by infection.…”

Section: The Epithelial Phasementioning

confidence: 99%

Mucosal barrier injury: biology, pathology, clinical counterparts and consequences of intensive treatment for haematological malignancy: an overview

Blijlevens¹,

Donnelly²,

Pauw³

2000

Bone Marrow Transplant

233

153

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Summary:Mucositis is an inevitable side-effect of the conditioning regimens used for haematopoietic stem cell transplantation. The condition is better referred to as mucosal barrier injury (MBI) since it is primarily the result of toxicity and is a complex and dynamic pathobiological process manifested not only in the mouth but also throughout the entire digestive tract. A model has been proposed for oral MBI and consists of four phases, namely inflammatory, epithelial, ulcerative and healing phases. A variety of factors are involved in causing and modulating MBI including the nature of the conditioning regimen, the elaboration of pro-inflammatory and other cytokines, translocation of the resident microflora and their products, for example, endotoxins across the mucosal barrier, exposure to antimicrobial agents and whether or not the haematopoietic stem cell graft is from a donor. Neutropenic typhlitis is the most severe gastrointestinal manifestation of MBI, but it also influences the occurrence of other major transplant-related complications including acute GVHD, veno-occlusive disease and systemic infections. The pathobiology, clinical counterparts and the means of measuring MBI are discussed together with potential approaches for prevention, amelioration and, perhaps, even cure. Bone Marrow Transplantation (2000) 25, 1269-1278. Keywords: mucositis; mucosal barrier injury; diagnosis; risk factors; treatment Mucositis is an inevitable side-effect of the intensive conditioning therapy used for haematopoietic stem cell transplantation 1 and usually refers to the mucosal ulceration of mouth and throat. However, it is generally accepted that oral mucositis is in reality the most obvious manifestation of damage or injury elsewhere particularly that of the gut. Hence, mucosal barrier injury (MBI) may be a more appropriate term for this biological process. There exists no clear definition of MBI which is defined by a constellation of signs and symptoms that vary in their clinical expression. Oral MBI is reported to affect 60% to 100% of transplant recipients 2,3 and is characterised by pain, oedema, erythema, lesions, pseudomembrane formation, excessive mucous production, reduced saliva and bleeding, all of which reduce the patient's ability to eat and drink. In contrast, there are no reliable data on the incidence of gut MBI although intestinal symptoms affect almost every transplant recipient to some extent and include nausea, vomiting, abdominal cramping and watery diarrhoea occasionally accompanied by macroscopic blood loss. The exact course and severity of bowel symptoms of MBI are also difficult to ascertain because many patients are in such pain due to oral MBI that they only gain relief from narcotic analgesia which induces constipation as a result of reduced gut motility. There are also a number of scoring systems for oral MBI 4 although none is universally accepted and all lack standardisation. As yet, there is no system for registering gut MBI although there are published definitions for grading toxicity o...

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“…Specifically, bacterial translocation is known to occur after abdominal surgery [5][6][7][8] (at higher rates if there is colon manipulation) 9 in patients with underlying bowel disease 10 and in critically ill patients, even if there is no bowel manipulation or preexisting bowel disease. 11,12 Hospital epidemiologists and infection preventionists now face an unnecessary dilemma when adjudicating whether a patient with bacteremia has a CLABSI or a secondary BSI. As a result of the issues raised above, we suspect that criteria used to determine whether there is a secondary source of infection vary from hospital to hospital.…”

mentioning

confidence: 99%

Current Definitions of Central Line–Associated Bloodstream Infection Is the Emperor Wearing Clothes?

Sexton

Chen

Anderson

2010

Infect. Control Hosp. Epidemiol.

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show abstract

Clinical significance of translocation.

Abstract: The gastrointestinal tract, besides being the organ responsible for nutrient absorption, is also a metabolic and immunological system, functioning as an effective barrier against endotoxin and bacteria in the intestinal lumen.

Cited by 262 publications

References 48 publications

Rhein inhibits lipopolysaccharide-induced intestinal injury during sepsis by blocking the toll-like receptor 4 nuclear factor-κB pathway

Rhein inhibits lipopolysaccharide-induced intestinal injury during sepsis by blocking the toll-like receptor 4 nuclear factor-κB pathway

Mucosal barrier injury: biology, pathology, clinical counterparts and consequences of intensive treatment for haematological malignancy: an overview

Current Definitions of Central Line–Associated Bloodstream Infection Is the Emperor Wearing Clothes?

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