Our laboratory studies how obesity-driven alterations in gut microbiota and hydrogen sulfide (H₂S) signaling reshape immune responses to worsen neuroinflammatory diseases, with a primary focus on severe multiple sclerosis (MS). Current projects investigate how obesity-induced gut dysbiosis drives CNS autoimmunity, how elevated microbial H₂S enhances protein sulfhydration and pro-inflammatory immune activity, and how disrupted GLP-1 receptor signaling contributes to heightened MS/EAE severity. We also translate these mechanistic findings to human MS by examining how obesity modulates immune responses, disease progression, and treatment outcomes. Together, these studies aim to identify microbiota- and H₂S-targeted therapeutic strategies tailored for obese individuals with MS.