Regular ArticlesABSENCE OF ENDOGENOUS INTERLEUKIN-6 ENHANCES THE INFLAMMATORY RESPONSE DURING ACUTE PANCREATITIS INDUCED BY CERULEIN IN MICE
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Cited by (47)
Organ Failure Due to Systemic Injury in Acute Pancreatitis
2019, GastroenterologyCitation Excerpt :Similarly, IL6 infusion in humans inhibited endotoxin induced TNF-α increase,128 and its long-term infusion led to hypoferremia and anemia,129,130 but not systemic injury. IL6131 and TNF-α132 have also been shown to have a protective role in AP, and neither these or other cytokines have been shown to induce OF.133–137 Therefore, targeting these cytokines alone may not improve outcomes in severe AP.
Immunopathogenesis of pancreatitis
2017, Mucosal ImmunologyImmune Mechanisms of Pancreatitis
2015, Mucosal Immunology: Fourth EditionLipolysis of visceral adipocyte triglyceride by pancreatic lipases converts mild acute pancreatitis to severe pancreatitis independent of necrosis and inflammation
2015, American Journal of PathologyCitation Excerpt :The improved survival with lipase inhibition suggests that the increased inflammatory response is a severity marker but not a severity mediator and is supported by the eventual reduction in serum cytokines in orlistat-treated mice electively sacrificed on the 5th day. Support for cytokines being SAP markers comes from the following: i) increases in serum IL-6 and tumor necrosis factor α secondary to UFAs,49 ii) mice administered IL-6 do not develop organ failure,65 iii) Il6 knockout mice develop SAP,65 iv) studies showing these cytokines have a protective role in AP and organ failure,66,67 and v) previous studies showing UFAs to up-regulate cytokines.35 Here we also note that the median necrosis was <10% in both the lean and ob/ob mice, similar to findings from previous reports,68 and is unaffected by lipase inhibition which prevents MSOF and mortality.
Interleukin-6 in inflammatory and malignant diseases of the pancreas
2014, Seminars in ImmunologyCitation Excerpt :Therapeutic approaches targeting the IL-6-trans-signaling/gp130/STAT3/CXCL1 signaling cascade during pancreatitis showed that its inhibition attenuates the systemic complications of severe AP significantly [102]. In keeping with these findings, administering a neutralizing antibody against IL-6 after the first cerulein injection effectively suppressed the increase in serum amylase and IL-6 levels, pancreatic local damage as well as systemic lung injury in mice with cerulein and LPS induced pancreatitis [116]. These data suggest that the IL-6-trans-signaling/gp130/STAT3/CXCL1 signaling cascade is a valid target for therapy of SAP with systemic complications.
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Correspondence to: Salvatore Cuzzocrea, Ph. D. Institute of Pharmacology, School of Medicine, University of Messina, Torre Biologica, Policlinico Universitario, Via C. Valeria Gazzi 98100, Messina, Italy. Tel: (39) 090 2213644; Fax: (39) 090 2213300; E-mail: [email protected]