Exploring Type 1 Diabetes Immunotherapy Using a Metabolically Engineered Brucella Melitensis 2439
Abstract Description The escalating global prevalence of diabetes presents a formidable health challenge, compounded by its associated complications such as retinopathy, neuropathy, diabetic ketoacidosis, and cardiovascular disease. Diabetes mellitus encompasses Type 1 (T1D) and Type 2, characterized by elevated blood glucose levels. T1D, an autoimmune disorder, arises from the body’s failure to produce insulin. Although conventional treatments rely on expensive oral medications or insulin therapy, the imperative for sustainable, alternative approaches is clear. The ongoing study explores bacterium-based immunotherapies as a promising avenue for T1D intervention. Specifically, we investigate the therapeutic potential of a metabolically engineered attenuated strain of Brucella melitensis 16MΔvjbR, denoted as BmΔvjbR::tnaA, in a spontaneous T1D murine model. Leveraging the immunomodulatory properties of this engineered bacterium, our objective is to restore insulin regulation and mitigate autoimmune responses underlying T1D pathogenesis. Through rigorous preclinical evaluation in murine models, our research aims to elucidate the efficacy and safety profile of BmΔvjbR::tnaA as a prospective therapeutic agent for T1D. This investigation not only broadens the therapeutic horizon for diabetes management but also underscores the potential of bacterium-based strategies in autoimmune disease interventions, paving the way for innovative and sustainable treatment modalities. Funding Sources NIH #1R01CA273002, ARPA-H #P0080 Topic Categories Therapeutic Approaches to Autoimmunity (THER)
Authors
- Kaylee Delgado (ORCID: https://orcid.org/0000-0002-8376-1416)
- Jim Jianxun Song
Institutions
- Mitchell Institute (US)
- Texas A&M University (US)
Publication Details
- Journal
- The Journal of Immunology
- Published
- 2025-11-01
- DOI
- https://doi.org/10.1093/jimmun/vkaf283.358
- Primary Topic
- Diabetes and associated disorders
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- National Institutes of Health
- National Institute on Aging