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Dual genetic absence of STAT6 and IL-10 does not abrogate anti-hyperglycemic effects of Schistosoma mansoni in streptozotocin-treated diabetic mice

Osada, Yoshio, Fujiyama, Tomohiro, Kamimura, Naoto, Kaji, Tsukushi, Nakae, Susumu, Sudo, Katsuko, Ishiwata, Kenji, Kanazawa, Tamotsu
Experimental parasitology 2017 v.177 pp. 1-12
Schistosoma mansoni, animal disease models, glycemic effect, hyperglycemia, insulin-dependent diabetes mellitus, interleukin-10, islets of Langerhans, lymph nodes, macrophages, mice, parasites, protective effect, spleen, streptozotocin
Schistosoma mansoni (Sm) is known to exert protective effects against various allergic and autoimmune disorders. It has been reported that this parasite protects NOD mice from spontaneous type 1 diabetes (T1D) and ameliorates streptozotocin (STZ)-induced T1D in wild-type mice. Here, we tried to clarify the anti-diabetic mechanisms of Sm in the latter model. Sm infection partially prevented the degradation of pancreatic islets and hyperglycemia in multiple low-dose (MLD) STZ-treated mice. Neither Treg cell depletion nor genetic absences of IL-10 and/or STAT6 abrogated the anti-hyperglycemic effects of Sm. Among M2 macrophage markers, Arg-1 and Ym1, but not Retnla, remained up-regulated in the pancreatic lymph nodes and in the spleens of STAT6/IL-10 double deficient (DKO) mice. Collectively, it is suggested that Sm exerts anti-diabetic effects on this experimental T1D model via Treg/IL-4/IL-13/IL-10-independent mechanisms. Augmented expressions of Arg-1 and Ym1 in the lymphoid organs adjacent to pancreas may be relevant to the anti-diabetic effects of Sm.