| Literature DB >> 25401425 |
Dietmar Zechner1, Marie Spitzner, Tassilo Müller-Graff, Brigitte Vollmar.
Abstract
Acute pancreatitis (AP) can lead to a systemic inflammatory response that often results in acute lung injury and single or multiple organ failure. In a previous study we demonstrated that diabetes aggravates the local pathophysiological process during AP. In this study we explore, if diabetes also increases pancreatitis induced systemic inflammation and causes lung injury. Acute pancreatitis was induced in untreated and streptozotocin-treated diabetic mice by injection of cerulein. Systemic inflammation was studied by IL-6 ELISA in blood plasma and white blood cell count. Lung inflammation and lung injury were quantified by chloroacetate esterase staining, evaluation of the alveolar cellularity index and cleaved caspase-3 immunohistochemistry. In normoglycaemic mice AP increased the IL-6 concentration in plasma and caused lymphocytopenia. Diabetes significantly increased the IL-6 concentration in plasma and further reduced the number of lymphocytes during AP, whereas diabetes had little effect on these parameters in the absence of pancreatitis. However, diabetes only marginally increased lung inflammation and did not lead to cell death of the lung epithelium during AP. We conclude that diabetes increases parameters of systemic inflammation during AP, but that this increase is insufficient to cause lung injury.Entities:
Keywords: acute lung injury; chloroacetate esterase staining; cleaved caspase-3; sepsis; systemic inflammatory response syndrome
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Year: 2014 PMID: 25401425 PMCID: PMC4285467 DOI: 10.1111/iep.12103
Source DB: PubMed Journal: Int J Exp Pathol ISSN: 0959-9673 Impact factor: 1.925