Effectiveness of interleukin-1 receptor antagonist (Anakinra) on cerulein-induced experimental acute pancreatitis in rats

Kaplan, Mustafa; Yazgan, Yusuf; Tanoğlu, Alpaslan; Berber, Ufuk; Öncü, Kemal; Kara, Muammer; Demırel, Dilaver; Kucuk, Irfan; Ozari, Halil Onur; İpçioğlu, Osman Metin

doi:10.3109/00365521.2014.926983

Cited by 18 publications

(15 citation statements)

References 25 publications

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“…Cytokines play a major role in the pathogenesis of respiratory complications that follow AP 6 . The neutralization and blockade of cytokines reduces the severity of AP and attenuates the systemic stress response in this disorder 9 41 42 43 . In our study, the loss of JAM-C also resulted in significantly higher levels of serum TNF-α and IL-6 in experimental pancreatitis.…”

Section: Discussionmentioning

confidence: 99%

Reverse-migrated neutrophils regulated by JAM-C are involved in acute pancreatitis-associated lung injury

Zeng

Fan

et al. 2016

Sci Rep

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Junctional adhesion molecule-C (JAM-C) plays a key role in the promotion of the reverse transendothelial migration (rTEM) of neutrophils, which contributes to the dissemination of systemic inflammation and to secondary organ damage. During acute pancreatitis (AP), systemic inflammatory responses lead to distant organ damage and typically result in acute lung injury (ALI). Here, we investigated the role of rTEM neutrophils in AP-associated ALI and the molecular mechanisms by which JAM-C regulates neutrophil rTEM in this disorder. In this study, rTEM neutrophils were identified in the peripheral blood both in murine model of AP and human patients with AP, which elevated with increased severity of lung injury. Pancreatic JAM-C was downregulated during murine experimental pancreatitis, whose expression levels were inversely correlated with both increased neutrophil rTEM and severity of lung injury. Knockout of JAM-C resulted in more severe lung injury and systemic inflammation. Significantly greater numbers of rTEM neutrophils were present both in the circulation and pulmonary vascular washout in JAM-C knockout mice with AP. This study demonstrates that during AP, neutrophils that are recruited to the pancreas may migrate back into the circulation and then contribute to ALI. JAM-C downregulation may contribute to AP-associated ALI via promoting neutrophil rTEM.

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Section: Discussionmentioning

confidence: 99%

Reverse-migrated neutrophils regulated by JAM-C are involved in acute pancreatitis-associated lung injury

Zeng

Fan

et al. 2016

Sci Rep

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“…Furthermore, we determined four main inflammatory mediators in the serum of SAP rats: TNF-α, IL-6, IL-1β, and IL-10. All of these cytokines were previously reported to participate in the acute-phase response of SAP (7,(22)(23)(24)(25). IL-6 was elevated more than the other cytokines in this SAP rat model.…”

Section: Il-6 Expression After Sap Inductionmentioning

confidence: 82%

Effects of Tocilizumab on Experimental Severe Acute Pancreatitis and Associated Acute Lung Injury

Chen

Yang

et al. 2016

Critical Care Medicine

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“…Studies have shown that IL-1β is significantly upregulated in the cerulein-induced acute pancreatitis model, suggesting that inflammatory cytokines are involved in the occurrence and development of pancreatitis 22 . Kaplan et al 23 found that the IL-1β receptor antagonist (Anakinra) could reduce the severity of acute pancreatitis. In this study, the levels of serum IL-1β and IL-6 in SAP mice were significantly higher than those in the control mice.…”

Section: Discussionmentioning

confidence: 99%

NLRP3 inflammasome inhibitor MCC950 can reduce the damage of pancreatic and intestinal barrier function in mice with acute pancreatitis

Shen

Yang

et al. 2022

Acta Cir. Bras.

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Purpose: Abnormal activation of NOD-like receptor protein 3 (NLRP3) inflammasome can lead to the occurrence and progression of acute pancreatitis. This study investigated the protective effect of MCC950 on pancreatitis mice. Methods: Eighteen mice were randomly divided into control group, severe acute pancreatitis (SAP) group and SAP+MCC950 group. Serum interleukin (IL)-1β, IL-6 and tumor necrosis factor-α (TNF-α) were measured by ELISA. Hematoxylin and eosin (HE) staining was used to evaluate the pathological damage. Western blotting was used to detect the expression of NLRP3 inflammasome and tight junction proteins in the small intestine and pancreas. Results: MCC950 could reduce the levels of IL-6 and IL-1β in SAP mice. After treatment with MCC950, the expression levels of NLRP3 inflammasome in the pancreas of SAP mice were significantly reduced and the pathological damage to the pancreas and intestine was alleviated. Compared with the control group, the expression of tight junction protein (ZO-1, occludin and claudin-4) in the intestinal mucosa of SAP mice was decreased, and the expression of claudin-4 and occludin were upregulated after MCC950 treatment. Conclusion: MCC950 can inhibit NLRP3 inflammasome activation and significantly reduce the inflammatory response and delay the process of pancreatitis. It has therapeutic potential in the treatment of acute pancreatitis.

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Effectiveness of interleukin-1 receptor antagonist (Anakinra) on cerulein-induced experimental acute pancreatitis in rats

Cited by 18 publications

References 25 publications

Reverse-migrated neutrophils regulated by JAM-C are involved in acute pancreatitis-associated lung injury

Reverse-migrated neutrophils regulated by JAM-C are involved in acute pancreatitis-associated lung injury

Effects of Tocilizumab on Experimental Severe Acute Pancreatitis and Associated Acute Lung Injury

NLRP3 inflammasome inhibitor MCC950 can reduce the damage of pancreatic and intestinal barrier function in mice with acute pancreatitis

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