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Journal of Student Scholarship

Journal of Student Scholarship

Abstract

Type 1 diabetes (T1D) is a chronic inflammatory autoimmune disease in which T cells destroy insulinproducing β cells in the pancreas, leading to hyperglycemia. Some T cells directly kill β cells, such as Tcytotoxic, or indirectly such as T-helper, while others, like regulatory T cells, actually protect them. A recent study showed that sodium bicarbonate (SB) exhibited anti-inflammatory activity by affecting immune cells other than T cells, implying its potential for the treatment of autoimmune diseases. Since SB has never been tested in an experimental mouse model for autoimmunity, we studied the effects of SB treatment on the development and severity of T1D, as well as on T cell subsets and T cell function. It was hypothesized that SB administration (200 mM, administered via drinking water) would decrease the incidence and severity of streptozotocin-induced T1D in 8-week-old C57BL/6 mice by its action on T cells. Glucose and body weight measurements were taken biweekly until mice were sacrificed four weeks later, and their spleens obtained for analysis of cell counts, viability, T cell proliferation, and quantification of T cell subsets by flow cytometry. There were no differences in splenic lymphocyte counts and viability between SB-treated and control mice. Although results showed that SB significantly decreased glucose levels and delayed diabetes development, it does not seem to affect the frequency of T cell populations nor their proliferation capacity. Our results suggest beneficial effects of SB in the prevention of mouse autoimmune T1D and highlight the need for further studies on its mechanism of action.

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