At the Shahi Lab, we investigate how obesity-driven changes in the gut microbiota and hydrogen sulfide (H₂S) signaling shape immune responses and worsen central nervous system (CNS) autoimmunity.
Our goal is to uncover mechanisms how obesity drive severe forms of multiple sclerosis (MS) and translate these findings into therapeutic strategies.
Current projects
Gut Microbiota and Obesity-Driven CNS Autoimmunity
Goal: To determine how obesity alters the gut microbiota to influence MS pathology and drive the severity of CNS autoimmune inflammatory disease.
Mechanistic Links Between Obesity, H₂S, and Neuroinflammation
Goal: To investigate how obesity-driven hydrogen sulfide production and altered neurotransmitter pathways enhance protein sulfhydration, promote pro-inflammatory immune activity, and drive severe autoimmune, inflammatory, and demyelinating diseases.
Obesity-Driven Modulation of GLP-1R and Its Impact on Immune Dysregulation and MS/EAE Severity
Goal: This project examines how obesity alters GLP-1R signaling to promote pro-inflammatory immune responses that worsen MS severity. By defining the obesity–GLP-1R axis, we aim to identify strategies to restore immune balance and improve therapeutic outcomes.
Translational MS Therapeutics
Goal: Based on our preclinical findings, this project investigates obesity-driven modulation of immune responses in MS patients to assess its impact on disease severity and treatment outcomes. This work lays the foundation for human subject–based studies and potential clinical trials, ultimately aiming to develop novel therapeutic strategies for obese individuals with MS.