Early increase in intestinal permeability in patients with severe acute pancreatitis: correlation with endotoxemia, organ failure, and mortality

Ammori, Basil J.; Leeder, Paul; King, R. F. G. J.; Barclay, G. R.; Martin, I. G.; Larvin, Michael; McMahon, Michael

doi:10.1016/s1091-255x(99)80067-5

Cited by 291 publications

(179 citation statements)

References 76 publications

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“…These findings may have clinical implications, because increased intestinal permeability has been shown to be associated with an increased risk of complications, MODS, or even mortality in critically ill patients (14)(15)(16)(17). The underlying mechanisms responsible for gut barrier dysfunction after HS/R are not fully understood, but increased production of certain proinflammatory mediators, such as IL-6 (11) or nitric oxide (18), may be involved.…”

Section: Introductionmentioning

confidence: 99%

Anti-HMGB1 Neutralizing Antibody Ameliorates Gut Barrier Dysfunction and Improves Survival after Hemorrhagic Shock

Yang

Harada

Mollen

et al. 2006

Mol Med

206

156

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Intestinal barrier dysfunction occurs following hemorrhagic shock and resuscitation (HS/R). High-mobility group B1 (HMGB1) has been shown to increase the permeability of Caco-2 human enterocyte-like epithelial monolayers in vitro. In this study, we found that serum concentrations of HMGB1 were higher in blood samples obtained from 25 trauma victims with hemorrhagic shock than in 9 normal volunteers. We also studied whether treatment with anti-HMGB1 antibody can ameliorate HS/R-induced gut barrier dysfunction in mice. Animals were shocked by withdrawal of blood to maintain mean arterial pressure at 25 to 30 mmHg for 2 h. After resuscitation with shed blood plus Ringer's lactate solution, the mice were treated with either anti-HMGB1 antibody or nonimmune rabbit IgG. Serum HMGB1 concentrations were significantly higher in trauma victims than control mice. Treatment with anti-HMGB1 antibody improved survival at 24 h and ameliorated the development of ileal mucosal hyperpermeability to FITC-labeled dextran. At 24 h after HS/R, treatment with anti-HMGB1 antibody decreased bacterial translocation to mesenteric lymph nodes and was associated with lower circulating concentrations of IL-6 and IL-10. These data support the notion that HMGB1 is a mediator of HS/R-induced gut barrier dysfunction and suggest that anti-HMGB1 antibodies warrant further evaluation as a therapeutic to ameliorate the morbidity of HS/R in trauma patients.

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Section: Introductionmentioning

confidence: 99%

Anti-HMGB1 Neutralizing Antibody Ameliorates Gut Barrier Dysfunction and Improves Survival after Hemorrhagic Shock

Yang

Harada

Mollen

et al. 2006

Mol Med

206

156

View full text Add to dashboard Cite

show abstract

“…The development of SAP is complicated and varied, triggered by local pathological pancreatic injuries, started the SIRS, aggravated by the gut, and resulted in exacerbating damage of systemic organs [11,12]. Excessive inflammatory response during SAP is the main cause of the intestinal mucosa injury, increased the permeability of intestinal mucosa, and aggravated the body invasion of intestinal bacteria continuously, which lead to bacterial translocation during inflammatory responses [13,14].…”

Section: Discussionmentioning

confidence: 99%

Emodin diminishes immune stress in rats with severe acute pancreatitis

Jin¹,

Zhang²,

Chen³

et al. 2018

biomedicalresearch

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Objectives: The aim was to observe the immune stress in rats with Severe Acute Pancreatitis (SAP) and diminish by emodin. Methods: Rats were divided into four groups: sham operation group (SO), SAP model group (SAP), emodin treatment group (ET), and two times dose emodin treatment group (HT). Samples of blood, terminal ileum and lung were harvested on 6 h, 12 h, 18 h and 24 h for examination. Serum amylase, and high-mobility group box 1 (HMGB 1), cyclooxygenase-2 (COX-2), and peroxisome proliferator activated receptor gamma-γ (PPAR-γ) in terminal ileum and lung was determined. Results: The values for emodin treated showed distinctly treatment effect, with lower levels of serum amylase, HMGB 1 and COX-2 on 12, 18 and 24 h and higher levels of PPAR-γ in the ET and HT groups compared with the SAP group on four time-points. The levels of detection indicators in the ET group were quite different from the HT group, with higher levels of serum amylase, HMGB 1 and COX-2 on 12, 18 and 24 h and lower expression of PPAR-γ on each time points. Conclusions: Emodin can diminish immune stress in rats with SAP. The strategy of two times may be a better therapeutic effect.

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“…During the early phase, dysregulation of the immunological reaction in SIRS dominates the pathological process and leads to circulatory disturbances and multiple organ dysfunction; during the late phase of the disease, the compensatory anti-inflammatory response syndrome (CARS) is highly likely to evoke infections (2,33,34). Multiple organ dysfunction and infection are the leading causes of mortality in severe acute pancreatitis (35)(36)(37)(38). Therefore, ameliorating the immune reaction of acute pancreatitis has been the focus of investigation over the last few years.…”

Section: Discussionmentioning

confidence: 99%

The regulatory role of immunosuppressants on immune abnormalities in acute pancreatitis

Duan

Chi

et al. 2013

Biomedical Reports

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Abstract. The uncontrolled progression of the inflammatory cascade is the main cause underlying the development of multiple organ dysfunction syndrome (MODS) in acute pancreatitis. In this study, we investigated the effects of several immunosuppressants on mitigating the systemic inflammatory reaction syndrome (SIRS) and the compensatory anti-inflammatory response syndrome (CARS) associated with acute pancreatitis. A total of 93 male Sprague Dawley rats were divided into 5 groups: group 1 was the sham group and group 2 underwent laparoscopic intrapancreatic duct injection of sodium taurocholate to induce pancreatitis. The remaining 3 groups were the same as group 2, with the addition of methylprednisolone, cyclophosphamide or methotrexate treatment (metastab, CTX or MTX groups, respectively). Following establishment of the acute pancreatitis model, the serum levels of inflammatory and anti-inflammatory cytokines in groups 2, 3, 4 and 5 were found to be significantly elevated. Following immunosuppressant administration, the levels of all inflammatory and anti-inflammatory cytokines investigated in groups 3, 4 and 5 were decreased compared to those in group 2. The pancreatic amylase levels and pancreatic wet weight (PWW) were also decreased in groups 3, 4 and 5 compared to those in group 2. Therefore, immunosuppressants may reduce inflammation-related cytokine levels in acute pancreatitis and relieve disease progression.

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Early increase in intestinal permeability in patients with severe acute pancreatitis: correlation with endotoxemia, organ failure, and mortality

Cited by 291 publications

References 76 publications

Anti-HMGB1 Neutralizing Antibody Ameliorates Gut Barrier Dysfunction and Improves Survival after Hemorrhagic Shock

Anti-HMGB1 Neutralizing Antibody Ameliorates Gut Barrier Dysfunction and Improves Survival after Hemorrhagic Shock

Emodin diminishes immune stress in rats with severe acute pancreatitis

The regulatory role of immunosuppressants on immune abnormalities in acute pancreatitis

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