ArticleInternational journal of experimental pathology2014
Diabetes increases pancreatitis induced systemic inflammation but has little effect on inflammation and cell death in the lung.
Article in International journal of experimental pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.
- Preexisting Diabetes Elevates Risk of Local and Systemic Complications in Acute Pancreatitis: Systematic Review and Meta-analysis.Pancreas · 2018Pooled it
- IRF5 regulates lung macrophages M2 polarization during severe acute pancreatitisWorld journal of gastroenterology · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
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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.
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