Lisa Ganley-Leal Ph.D.
Office: 650 Albany St, X-6
Dr. Ganley-Leal’s laboratory focuses on defining the role of B cells and systemic TLR ligands in human chronic inflammatory disease. Chronic inflammatory diseases, including classic inflammatory and primarily metabolic, or infectious, appear to have similar systemic inflammatory mechanisms despite clinical heterogeneity. Thus, a “leaky gut” or translocation of endotoxin into the blood stream links diseases such as inflammatory bowel disease (IBD), diabetes, and obesity related insulin resistance and schistosomiasis. Increased endotoxin in the blood stream leads to the release of other inflammatory mediators, including HMGB1, an endogenous TLR ligand. Circulating B cells in chronic inflammatory disease patients have increased levels of surface TLR2 and TLR4 and exhibit the potential to modulate inflammation through the production of IL-8 and other mediators. HMBG1 appears to function similar to TLR2 ligands for B cells and stimulates the production of chemokines. However, despite surface TLR4 expression, patient B cells fail to respond to E. coli LPS. Rather, B cells respond to LPS species with different structures, such those which are considered antagonistic for myeloid TLR4. Dr Ganley-Leal’s group is focused on defining these unique functions of human B cells and how they relate to patient health. The laboratory collaborates with clinicians in gastroenterology and endocrinology at the BUSM including Drs. Van Dyke and McDonnell to better understand how this systemic microbial assault leads to chronic stimulation of the immune system and patient morbidity.