Bernardo Ortega

Bernardo Ortega, Ph.D

Associate Professor
(585) 395-5190
Office: Lennon Hall 217


Our research aims at understanding the mechanisms regulating magnesium metabolism in the human body. Common diseases such as ulcerative colitis are affected by dietary magnesium. Using a mouse model of ulcerative colitis, we try to understand the role of magnesium intake in regulating the composition of the intestinal microbiome in healthy and diseased mice.

Research Interests

Ulcerative colitis (UC) frequently results in magnesium (Mg) malabsorption leading to hypomagnesemia or low level of magnesium in plasma. Mg deficiency induces a proinflammatory state that has been proposed to worsen UC, but the mechanism is unknown. Here we hypothesize that a relation may exist between Mg intake and the composition of the bacterial flora of the intestine, which ultimately may contribute to aggravating UC. Associated with UC are important changes in the permeability of the intestine, the composition of the bacterial flora of the intestine, and how the immune system recognizes them. Experiments in our lab show that Mg deprivation in mice induces hypomagnesemia, but also results in important changes in the composition of the flora of the intestine, specifically lactic acid bacteria and Bifidobacterium. These changes could be the result of alterations in the function of the gastrointestinal (GI) tract induced by Mg deficiency and inflammation. However, unlike humans, Mg is the most important divalent cation for bacteria, and thus Mg availability is also important for bacterial proliferation, with some bacteria being able to compete better than others. This research proposal aims at understanding how dietary Mg may be determining the composition of the GI flora, and thus influencing evolution and remission of UC.

A first aim is to understand how Mg deprivation affects proliferation of intestinal bacteria. Mice will be deprived of Mg in their diets, while one experimental group will receive the normal Mg daily intake via subcutaneous pumps. Changes in the bacterial composition of the gut will be analyzed using state-of-the-art next-generation bacterial DNA sequencing. The study will compare GI bacterial populations of mice deprived of Mg, with those having normal dietary or subcutaneous Mg intake. This aim will allow us to understand if changes in the composition of the intestinal flora are dependent on low serum Mg, or if instead Mg availability in the lumen of the intestine determines which bacteria proliferate best. A second aim will investigate if Mg intake influences intestinal permeability and/or systemic infection in a chemically-induced mouse model of UC (Dextran Sodium Sulfate, or DSS). We will first investigate the changes in intestinal permeability induced by DSS treatment, and then use next-generation DNA sequencing performed on samples from mouse spleen in order to investigate which bacterial strains are more capable of invading the host. We anticipate that Mg may limit systemic bacterial infection due to an improved gastrointestinal barrier, but we also expect that Mg deprivation may drive some bacteria into a more pathogenic state, as has been previously described for Salmonella, rendering them more capable of systemic infection.

Lessons from this animal study may help in the design of future studies aiming at guiding sustainable dietary modifications in human patients in order to achieve and maintain remission.