The risk for development of metabolic and cardiovascular diseases in later life is increasing, as the population is becoming overweight and obese at earlier ages. Early-life nutritional programming influences late-life disease susceptibility across generations, in part through epigenetic mechanisms including DNA methylation. Much of the immune system is developed in utero and is therefore potentially susceptible to the influence of prenatal environmental factors. Using mouse models, it has been shown that prenatal diet rich in methyl donors (L-methionine, vitamin B-12, folic acid, choline, betaine, zinc) can increase airway reactivity and worsen inflammatory bowel disease but improves cardiovascular disease outcomes in F1 mice. These studies established that the prenatal methyl donor diet does incur immunological changes that impact offspring health. Our lab has shown that early nutrition in the form of a prenatal methyl diet increases global CD3+ T cell methylation in ApoE (-/-) mice, and we had further determined that this epigenetic effect suppresses the activity of T cell chemokine receptors which play a key role in the pathogenesis of atherosclerotic lesion inflammation. Our lab has also previously established that endoplasmic reticulum (ER) stress is increased in old macrophages, and more interestingly, upon alleviating this ER stress with a chemical chaperone, inflammatory cytokine production by old macrophages decreases to comparable levels to that of young macrophages. From this knowledge, we are investigating how the methyl donor diet impacts later-life obesity and obesity-induced inflammation in adipose tissue and adipose tissue macrophages.
2017 Microbiome Explorer Program, research support (U of M Host Microbiome Initiative)
2016 The American Association of Immunologists (AAI) Trainee Abstract Award • Rackham Conference Travel Grant (U of M)
2015-17 Career Training in the Biology of Aging Training Grant (NIH T32)
2014-15 Research Training in Experimental Immunology Training Grant (NIH T32)
2014 Ethiopia-Michigan Platform for Advancing Collaborative Engagement Travel Grant (U of M)
2010-13 Laurels Scholarship (PSU University Honors merit-based tuition-waiver scholarship) 2012 • Intercultural Leadership (PSU International Student Mentors Program)
Eckley, S, Mau, T, Hoenerhoff, M, Bergin, I, Yung, R, and Villano, J. “An outbreak of Clostridium difficile in a colony of C57BL/6J mice.” American Association for Laboratory Animal Science, October 15-19, 2017, Austin, TX. PS103.
Presenter (Oral & Poster): Mau, T, Ghosh, AK, O'Brien, M, Zamarron, B, Delproposto, J, Lumeng, C, and Yung, R. “Prenatal methyl-donor supplemented diet increases endoplasmic reticulum stress and inflammation in adipose tissue CD11b+ cells in F1 mice.” The American Association of Immunologists 2016 Annual Meeting, May 13-17, 2016, Seattle, WA. Presented as poster: U of M Internal Medicine Research Symposium, May 18-20, 2016 and Geriatrics Center Research Symposium, May 23, 2016, Ann Arbor, MI. 15th Annual Immunology Retreat, June 3-4, 2016, Maumee Bay Lodge and Conference Center, OH.
Ghosh, AK, Garg, SK, Mau, T, O’Brien, M, Yung, R. “Impaired autophagy activity is associated with elevated ER-stress and inflammation in aging adipose tissue derived cells.” National Pepper Center Meeting 2016, Washington DC. Presented as poster: Annual Geriatrics Center Symposium 2016 and 24th Annual Department of Internal Medicine Research Symposium, May 2016, Ann Arbor, MI.
Ghosh, AK, Garg, SK, Mau, T, O’Brien M, Liu J, and Yung R. “Elevated Endoplasmic Reticulum (ER)-stress response contributes to adipose tissue inflammation in aging.” Geriatrics Center Research Symposium 2014, Ann Arbor, MI.