Early Gut Barrier Dysfunction in Patients with Severe Acute Pancreatitis: Attenuated by Continuous Blood Purification Treatment

Zhang, Jianbin; Yuan, Chao; Gan, Hua; Tong, Ruyan; Luo, Xiangfeng; Zhou, Ying

doi:10.1177/039139881003301003

Cited by 36 publications

(40 citation statements)

References 21 publications

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“…A former study has proved that CBP could ameliorate the prognosis of patients suffering from MOF via unknown mechanisms, which was in accordance with our results [16]. CBP can not only improve the general conditions but also effectively improve gut barrier dysfunction, whose beneficial effect on gut barrier dysfunction is associated with the improvement of cytoskeletal instability, by down-regulating iNOS through the removal of excess proinflammatory factors [25]. Another data showed that after CBP treatment, endothelial hyperpermeability induced by serum from severe acute pancreatitis (SAP) patients with lung injury was ameliorated [26].…”

Section: Discussionsupporting

confidence: 91%

Continuous Blood Purification Ameliorates Multiple Organ Failure Through Inhibiting the Activation of the P38 MAPK Signaling Pathway in a Rat Model

Ling

Wen

Zhang

et al. 2018

Kidney Blood Press Res

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Background/Aims: Multiple organ failure (MOF) is a primary threat to the survival of patients with systemic inflammation. Blood purification is employed in the treatment of MOF, as an artificial kidney or artificial liver. This study focuses on the effects of continuous blood purification (CBP) on ameliorating MOF through regulating the p38 mitogen-activated protein kinase (MAPK) signaling pathway in a rat model. Methods: A rat model of MOF was successfully established by endotoxin injection after hemorrhagic shock resuscitation. The mRNA expressions of inducible nitric oxide synthase (iNOS) and p38 MAPK of liver, kidney, and lung tissues in each group were measured by RT-qPCR at each measuring time point. To evaluate the activation of p38 MAPK signaling pathway, protein levels of phosphorylated p38 (p-p38) MAPK and p38 MAPK was measured by western blot analysis. The serum levels of nitric oxide and TNF-α were determined. Results: After CBP treatment, the levels of SGPT, SGOT, Cr, and BUN were significantly declined, while the PaO₂ value was increased. Expressions of p38 MAPK mRNA, iNOS mRNA, p-p38 MAPK protein and p38 MAPK protein, and nitric oxide and TNF-α levels were markedly elevated in MOF, an effect blunted by CPB. Meanwhile, pathological sections of liver, kidney, and lung tissues after CPB treatment ameliorated swelling and inflammation. Conclusion: Our study proved that CBP could downregulate the p38 MAPK signaling pathway, suppress iNOS expression, reduced the serum levels of nitric oxide and TNF-α, thus ameliorate symptom of MOF.

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Section: Discussionsupporting

confidence: 91%

Continuous Blood Purification Ameliorates Multiple Organ Failure Through Inhibiting the Activation of the P38 MAPK Signaling Pathway in a Rat Model

Ling

Wen

Zhang

et al. 2018

Kidney Blood Press Res

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“…Although the complete sets of mRNAs and processes controlled by H19 in the intestinal epithelium remain to be fully elucidated, the fact that the prevention of miR-675 processing from H19 by HuR protected the epithelial barrier function highlights the impact of an individual lncRNA in controlling gut permeability in specific clinical settings. These findings are particularly significant in patients with traumatic damage, thermal injury, or shock and in patients recovering from major surgical operations, as acute gut barrier dysfunction occurs commonly in these clinical situations (12,64). In summary, our results indicate that the H19/ miR-675 axis downregulates the intestinal barrier function by inhibiting ZO-1 and E-cadherin expression posttranscriptionally, whereas HuR prevents miR-675 processing from H19 and is crucial for maintaining a normal barrier function under biological and pathological conditions.…”

Section: Discussionmentioning

confidence: 99%

H19 Long Noncoding RNA Regulates Intestinal Epithelial Barrier Function via MicroRNA 675 by Interacting with RNA-Binding Protein HuR

Zou

Jaladanki

Liu

et al. 2016

Molecular and Cellular Biology

135

118

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The disruption of the intestinal epithelial barrier function occurs commonly in various pathologies, but the exact mechanisms responsible are unclear. The H19 long noncoding RNA (lncRNA) regulates the expression of different genes and has been implicated in human genetic disorders and cancer. Here, we report that H19 plays an important role in controlling the intestinal epithelial barrier function by serving as a precursor for microRNA 675 (miR-675). H19 overexpression increased the cellular abundance of miR-675, which in turn destabilized and repressed the translation of mRNAs encoding tight junction protein ZO-1 and adherens junction E-cadherin, resulting in the dysfunction of the epithelial barrier. Increasing the level of the RNA-binding protein HuR in cells overexpressing H19 prevented the stimulation of miR-675 processing from H19, promoted ZO-1 and E-cadherin expression, and restored the epithelial barrier function to a nearly normal level. In contrast, the targeted deletion of HuR in intestinal epithelial cells enhanced miR-675 production in the mucosa and delayed the recovery of the gut barrier function after exposure to mesenteric ischemia/reperfusion. These results indicate that H19 interacts with HuR and regulates the intestinal epithelial barrier function via the H19-encoded miR-675 by altering ZO-1 and E-cadherin expression posttranscriptionally.T he majority of the mammalian genome is transcribed into a vast number of noncoding RNAs, whereas protein-coding transcripts account for only a minority of transcriptional output (1, 2). Long noncoding RNAs (lncRNAs) are defined as transcribed RNAs spanning Ͼ200 nucleotides in length that lack protein-coding capacity and are distinct from well-characterized structural RNAs (rRNAs, tRNAs, snRNAs, and snoRNAs) or small regulatory RNAs (3, 4). lncRNAs arise from intergenic, antisense, or promoter-proximal regions, and they share many features with mRNAs. Both classes of RNA can be transcribed from multiexonic genes and possess a 5=-methyl-guanosine cap and 3=-poly(A) tail (1,3,5). Some lncRNAs are ubiquitous, but others are dynamically expressed in tissue-, differentiation stage-, and cell type-specific patterns (4, 6). lncRNAs have been involved in a variety of cellular functions, physiologic processes, and disease states by modulating gene expression at different levels, including chromatin remodeling, transcriptional and posttranscriptional control, and protein metabolism (1, 3, 4). lncRNAs can serve as repressors or activators of gene transcription, as has been extensively reported (1, 4), but lncRNAs also can regulate mRNA decay and translation, working jointly with microRNAs (miRNAs) and RNA-binding proteins (RBPs) (7-9).Intercellular junction complexes, comprising tight junctions (TJs) and adherens junctions (AJs), fence the paracellular space in simple epithelia, such as those lining the intestine, kidneys, and lung, and form an important barrier against a wide array of noxious substances present in the lumen (10, 11). In the intestine, the disruption...

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“…However, since inflammatory mediators play a role in pathogenesis of both septic and non-septic systemic inflammatory response syndromes, HCO-CVVHDF may be useful in either sterile or infected SAP. Moreover, there is evidence that cytokine removal can improve gut barrier function in patients with SAP [15], which could potentially prevent bacterial translocation, bacteremia and infection of necrotic tissues. There is also evidence that HCO-CVVHDF may restore native immunity competence and T-lymphocyte function, thus improving antibacterial immunity and contributing to prevent infective complications and late mortality [12].…”

Section: Discussionmentioning

confidence: 99%

Use of Continuous Venovenous Hemodiafiltration with a High Cutoff Membrane in a Patient with Severe Acute Pancreatitis

Chelazzi¹,

Giugni²,

Giannoni³

et al. 2012

OJNeph

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In patients with severe acute pancreatitis (SAP) early and persistent elevated circulating levels of interleukins (IL)-1, 2 and 6 and tumor necrosis factor (TNF)-α are linked to severity of disease and early multiple organ failure (MOF), while persistently elevated serum IL-10 is linked to immune paralysis and infectious complications. Although experimental and clinical evidence exists that continuous venovenous hemodiafiltration with high cutoff membranes (HCO-CVVHDF) efficiently removes inflammatory mediators from blood of patients with severe sepsis or septic shock, data are lacking on the subset of patients with SAP, particularly in cases with uninfected necrosis. We treated with HCO-CVVHDF a 59-year-old man admitted to our intensive care unit (ICU) with SAP inducing early-onset cardiovascular, respiratory and renal dysfunctions associated with high circulating levels of IL-6 and TNF-α and without overt clinical or laboratory signs of infection. During the treatment, cardiovascular, respiratory and renal functions rapidly normalized and circulating levels of IL-6 and TNF-α consistently decreased. The patient was discharged from ICU on day 20.

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Early Gut Barrier Dysfunction in Patients with Severe Acute Pancreatitis: Attenuated by Continuous Blood Purification Treatment

Cited by 36 publications

References 21 publications

Continuous Blood Purification Ameliorates Multiple Organ Failure Through Inhibiting the Activation of the P38 MAPK Signaling Pathway in a Rat Model

Continuous Blood Purification Ameliorates Multiple Organ Failure Through Inhibiting the Activation of the P38 MAPK Signaling Pathway in a Rat Model

H19 Long Noncoding RNA Regulates Intestinal Epithelial Barrier Function via MicroRNA 675 by Interacting with RNA-Binding Protein HuR

Use of Continuous Venovenous Hemodiafiltration with a High Cutoff Membrane in a Patient with Severe Acute Pancreatitis

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