Impact of acute schistosomiasis mansoni and concurrent type 1 diabetes on pancreatic architecture in mice

Abstract

It is not well understood how type 1 diabetes (T1D) and concomitant acute schistosomiasis mansoni affect pancreatic architecture. Male Swiss mice were administered streptozotocin (single 100 mg/kg i.p.) and thirty days later infected with 80 Schistosoma mansoni cercariae. Mice were divided into groups (n = 5): A (healthy control), B (infected), C (uninfected diabetic), and D (diabetic + infected) and euthanized at week 9 post-infection. Blood glucose levels, biometry, stereology, and pancreatic histology were evaluated. Groups C and D showed hyperglycemia (>200 mg/dL). Group B had a higher (+79%) pancreatic mass than A. The endocrine pancreas showed fewer islets of Langerhans (−62%; −50%) and a smaller islet area (−36%; −30%) in C and D, respectively, compared to A. Group D had a smaller (−37%) islet area than B. The volume density of the islets was reduced (−33%) in group C compared to A. Within the exocrine pancreas, the volume density of the pancreatic parenchyma was reduced in groups B (−29%) and D (−26%), and increased in C (+15%) compared to A. Group D was reduced (−35%) compared to C. Group D showed generalized pancreatitis, including disrupted tissue with multiple nuclei of destroyed acinar cells and lost connective tissue and acinar cells with a paucity of zymogen granules. Pancreatic stellate cells were found around areas of distorted architecture. Paired adult worms were found within the pancreatic vessels. In conclusion, concomitant T1D and schistosomiasis mansoni promote extensive exocrine and endocrine changes in the pancreas, whereas pancreatic involvement begins in acute schistosomiasis.