Nuclear Factor Kappa B Expression in Peripheral Blood Mononuclear Cells of Patients with Acute Pancreatitis

Satoh, Akihiko; Masamune, Atsushi; Kimura, Kenji; Kaneko, Kenzo; Sakai, Yoshitaka; Yamagiwa, Tetsuya; Satoh, Masahiro; Kikuta, Kazuhiro; Asakura, Tadashi; Shimosegawa, Tooru

doi:10.1097/00006676-200305000-00007

Cited by 33 publications

(25 citation statements)

References 42 publications

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“…Only two reports have investigated NF-ĸB activation in human acute pancreatitis. Satoh et al [17] found significantly higher levels of NF-ĸB activation in PBMNCs at admission, similar to our study. On the other hand, O’Reilly et al [34] recently detected significantly increased NF-ĸB activation in PBMNCs of acute pancreatitis patients within 24 h of symptom onset.…”

Section: Discussionsupporting

confidence: 92%

“…PBMNCs were isolated from blood using a modification of the method described by Satoh et al [17]. Commercial kit (Chemicon’s Transcription Factor Assay Kit Cat No.…”

Section: Methodsmentioning

confidence: 99%

“…NF-ĸB activation has been demonstrated in experimental pancreatitis induced by cholecystokinin, taurocholate, bile-pancreatic duct ligation, L -arginine, and active REL/p65 and in human pancreatitis in pancreatic tissue, lung, liver, peripheral blood mononuclear cells (PBMNCs), peritoneal and alveolar macrophages, and endothelial cells [15,16,17,18]. NF-ĸB occupies a critical position in the inflammatory cascade, especially in acute pancreatitis, and it consequently has received much attention as a potential target for diagnosis, therapy and prognosis.…”

Section: Introductionmentioning

confidence: 99%

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Does Nuclear Factor-Kappa B in Peripheral Mononuclear Cells Have a Prognostic Role during Acute Necrotizing Pancreatitis in Rats?

Alhan

Türkyılmaz²,

Erçín³

et al. 2011

Eur Surg Res

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Aim: To investigate the prognostic role of nuclear factor-kappa B (NF-ĸB) activity in peripheral blood mononuclear cells (PBMNCs) during acute necrotizing pancreatitis (ANP) in rats. Methods: ANP was induced by an intravenous infusion of cerulein over 6 h superimposed on glycodeoxycholic acid (10 mmol/l) into the biliary-pancreatic duct for 10 min. The rats were divided into five groups and the first group served as the control. ANP was induced in the remaining groups, which were followed for 6, 12, 24 and 48 h. The mortality rate, serum amylase, alanine transferase (ALT), urea, creatinine and calcium, pancreatic histology, and NF-ĸB activity in PBMNCs were investigated. The NF-ĸB activity in PBMNCs was measured as two subunits of NF-ĸB, p50 and p65. Results: A significant increase in mortality rate, pancreatic damage, serum activity of amylase and ALT, urea and NF-ĸB p65 activity in PBMNCs were observed. There was a significant correlation between the mortality rate and pancreatic damage in conjunction with time, but there was no correlation between NF-ĸB p65 activity in PBMNCs and the mortality rate. Conclusion: The measurement of p65 levels of NF-kB in PBMNCs has no prognostic role during ANP in rats.

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Section: Discussionsupporting

confidence: 92%

“…PBMNCs were isolated from blood using a modification of the method described by Satoh et al [17]. Commercial kit (Chemicon’s Transcription Factor Assay Kit Cat No.…”

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Does Nuclear Factor-Kappa B in Peripheral Mononuclear Cells Have a Prognostic Role during Acute Necrotizing Pancreatitis in Rats?

Alhan

Türkyılmaz²,

Erçín³

et al. 2011

Eur Surg Res

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“…In the present study, apelin-induced reductions of pancreatic ECM protein levels were associated temporally with apelininduced reductions in pancreatic NF-B activation, implying that apelin's induced reductions in pancreatic ECM levels are linked to its inhibition of NF-B activation. Interestingly, evidence of NF-B involvement in human AP has been reported (40).…”

Section: G146 Apelin and Pancreatitismentioning

confidence: 99%

Pancreatitis activates pancreatic apelin-APJ axis in mice

Han

Englander

Gómez

et al. 2013

American Journal of Physiology-Gastrointestinal and Liver Physi

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Pancreatitis is classified into acute pancreatitis (AP) and chronic pancreatitis (CP). Apelin, a small regulatory peptide, is the endogenous ligand for the APJ receptor. Apelin and APJ are expressed in the pancreas. The aims of this study were to examine whether apelin influences the inflammatory and fibrosis responses to pancreatitis in mice and to identify mechanisms behind apelin's activities. Supramaximal cerulein induction of AP or CP caused significant ( P < 0.05) elevations in pancreatic apelin and APJ expression. Levels declined during the recovery phases. In apelin gene-knockout mice with pancreatitis, pancreatic neutrophil invasion and myeloperoxidase activity were enhanced significantly, and apelin treatment suppressed both. Apelin exposure reduced CP-induced elevations of extracellular matrix-associated proteins. Apelin inhibited PDGF-simulated connective tissue growth factor production and proliferation of pancreatic stellate cells (PSCs). Serum granulocyte colony-stimulating factor and keratinocyte cytokine levels were higher in apelin gene-knockout than wild-type mice with pancreatitis. Apelin reduced AP- and CP-induced elevations in pancreatic NF-κB activation. Together, these findings imply that the pancreatic apelin-APJ system functions to curb the inflammatory and fibrosis responses during pancreatitis. Furthermore, findings suggest that apelin reduces inflammation and fibrosis by reducing neutrophil recruitment and PSC activity. Inhibition of neutrophil invasion may be mediated by reduced keratinocyte cytokine and granulocyte colony-stimulating factor secretion. Apelin-induced reductions in PSC proliferation and connective tissue growth factor production are putative mechanisms underlying apelin's inhibition of extracellular matrix production. The apelin-associated changes in NF-κB binding may be linked to apelin's regulation of pancreatic inflammatory and fibrosis responses during pancreatitis.

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“…Although the exact pathogenesis remains unclear [4] . Studies in recent years have found that NF-κB (nuclear factor kappa-B) which is a main factor in the genetic transcription of inflammation, presents high expression state in acute pancreatitis and plays an important role in the onset and turnover of acute pancreatitis together with other inflammatory cytokines [5][6][7] . Dexamethasone is the antagonist of a nonspecific inflammatory mediator [8] .…”

Section: Introductionmentioning

confidence: 99%

Influence of dexamethasone on inflammatory mediators and NF-κB expression in multiple organs of rats with severe acute pancreatitis

Zhang

Zhang²,

Chen³

et al. 2007

WJG

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A I M :To o b s e r v e t h e t h e r a p e u t i c e f f e c t s o f dexamethasone on rats with severe acute pancreatitis (SAP) and investigate the influences of dexamethasone on the inflammatory mediators and NF-κB expression in multiple organs of SAP rats as well as the mechanisms involved. METHODS:Ninety Sprague-Dawley (SD) rats with SAP were randomly divided into the model group (n = 45) and dexamethasone treatment group (n = 45), and another 45 rats were selected for the sham operation group. All groups were randomly subdivided into the 3 h, 6 h and 12 h groups, each group containing 15 rats. The survival of all groups and pathological changes of multiple organs (liver, kidney and lung) were observed at different time points after the operation. The pathological score of multiple organs was carried out, followed by the determination of amylase, endotoxin and TNF-α contents in blood. The tissue microarray was used to detect the expression levels of NF-κB p65 protein in multiple organs. RESULTS:There was no marked difference between the model group and treatment group in the survival rate. The amylase content of the treatment group was significantly lower compared to the model group at 12 h (P < 0.01, 7791.00 vs 9195.00). Moreover, the endotoxin and TNF-α levels of the treatment group were significantly lower than that of the model group at 6 h and 12 h (P < 0.01, 0.040 vs 0.055, 0.042 vs 0.059 and P < 0.05, 58.30 vs 77.54, 38.70 vs 67.30, respectively).Regarding the changes in liver NF-κB expression, the model group significantly exceeded the sham operation group at 3 h (P < 0.01, 1.00 vs 0.00), and the treatment group significantly exceeded the sham operation group at 12 h (P < 0.01, 1.00 vs 0.00), whereas no marked difference was observed between the model group and treatment group at all time points. The kidney NF-κB expression level in the treatment group significantly exceeded the model group (P < 0.05, 2.00 vs 0.00) and the sham operation group (P < 0.01, 2.00 vs 0.00) at 12 h.No NF-κB expression in the lung was found in any group. CONCLUSION:Dexamethasone can lower the amylase, endotoxin and TNF-α levels as well as mortality of SAP rats. NF-κB plays an important role in multiple organ injury. Further studies should be conducted to determine whether dexamethasone can ameliorate the pathological changes of multiple organs by reducing the NF-κB expression in the liver and kidney. The advantages of tissue microarrays in pancreatitis pathological examination include time-and energy-saving, and are highly efficient and representative. The restriction of tissue microarrays on the representation of tissues to various extents due to small diameter may lead to the deviation of analysis. treatment group was injected once with dexamethasone (1 mL = 5 mg) via the vena caudalis, 0.5 mg/100 g body weight 15 min after successful preparation of SAP model. During the laparotomy in the sham operation group, we performed pancreas and duodenum manipulation, observed pathological changes of multiple organs and fi...

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Nuclear Factor Kappa B Expression in Peripheral Blood Mononuclear Cells of Patients with Acute Pancreatitis

Abstract: An alteration of the characteristics of PBMCs occurs in the early phase of acute pancreatitis and may predispose patients to a higher risk of serious systemic complications.

Cited by 33 publications

References 42 publications

Does Nuclear Factor-Kappa B in Peripheral Mononuclear Cells Have a Prognostic Role during Acute Necrotizing Pancreatitis in Rats?

Does Nuclear Factor-Kappa B in Peripheral Mononuclear Cells Have a Prognostic Role during Acute Necrotizing Pancreatitis in Rats?

Pancreatitis activates pancreatic apelin-APJ axis in mice

Influence of dexamethasone on inflammatory mediators and NF-κB expression in multiple organs of rats with severe acute pancreatitis

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