Emergency BU Alert BU Medical Campus OPEN Jan. 28, 2015 Boston University Medical Campus will be open Wednesday, Jan. 28, 2015. BUSM classes will be held as scheduled. Staff should check with their managers regarding work schedules. Medical, PA and GMS students who are assigned to inpatient services or clinics are expected to be present, if possible. Students who are assigned to outpatient services should check with their course director or the policy at the clinical site. GMS classes are canceled. Staff should check with their manager regarding their work schedules. The Henry M. Goldman School of Dental Medicine will follow normal school hours. All Patient Treatment Centers will be open for patient care and all classes will be held as scheduled. BU School of Public Health classes are canceled; SPH non-essential staff may telecommute. Employees who are part of the BUMC parking program should park in your assigned lot or garage. The Boston parking ban is still in effect. For updated information, please call the weather/emergency hotline at 617-638-6886 or visit the BU Emergency Communications website at http://www.bu.edu/ehs/comm/

Lisa Ganley-Leal Ph.D.

Medicine-Infectious Diseases

Office: 650 Albany St, X-6
Phone: 617-414-7234
Email: lmgleal@bu.edu

Research:

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.

Affiliated Websites:

Infectious Diseases Webpage