Gail A.M. Cresci,  Ph.D.

Gail A.M. Cresci, Ph.D.


Lerner Research Institute, 9500 Euclid Avenue, Cleveland, Ohio 44195
Location: NB2-109
Phone: (216) 445-8317


Our research focuses on the gut microbiota, centering on clinical situations in which gut dysbiosis occurs with investigations targeting alterations in metabolic byproducts of the gut microbiota. Taking a nutritional therapeutic approach, our ultimate goal is to discover and develop therapies to maintain or restore digestive and gut health that is altered during gut dysbiosis and associated pathologies.

The human intestine houses trillions of commensal bacteria (gut microbiota) dominated by nearly 800 different species. “Healthy” gut microbiota supports epithelial cell health, nutrient metabolism and breakdown, and indirect mucosal defense against pathogenic bacteria. Gut microbiota ferment non-digestible polysaccharides to yield short-chain fatty acids (SCFA), acetate, propionate, and butyrate. Butyrate is the most dynamic SCFA and important for intestinal health. In addition to serving as the primary fuel source for colonocytes, butyrate maintains gut integrity, modulates inflammation and immune function. Without butyrate, intestinal tissue is vulnerable to apoptosis, inflammation, mucosal atrophy and colonic pathology. Our recent work has investigated two known modalities known to induce gut dysbiosis, antibiotic therapy and ethanol consumption. In both these mouse models, oral supplementation with butyrate, in the form of tributyrin, mitigated intestinal injury, maintaining expression of nutrient receptors and transporters as well as preserving intestinal barrier function. Additionally, in the ethanol model, intestinal protection was associated with reduced liver injury. Developing data investigates a targeted approach to positively affect gut luminal butyrate levels and prevent injury through provision of designer synbiotics.

One of our major goals is to identify and characterize the microbial and metabolomic signature associated with the progression of pathologies including alcoholic and non-alcoholic fatty liver disease, chemotherapy-induced mucositis, as well as clinical outcomes and organ integrity in liver and intestinal organ transplant patients and in premature infants.

04/13/2018 |  

Preventing a Common Hospital-Acquired Infection

Clostridium difficile (CD), or C. diff as it is sometimes called, is a common hospital-acquired pathogen that leads to CD infection (CDI), which increases the risk for patient illness and death and raises healthcare costs. CD thrives when a patient's microbial balance—the amount of "good" versus "bad" bacteria—is altered, as happens in response to antibiotics. Patients taking long-term antibiotics are at high-risk of CDI. Currently, the standard-of-care method to prevent CDI is simply to avoid prescribing inappropriate or unnecessary antibiotics.