Pediatrics Assistant Professor
Pediatrics Associate Professor, Microbial Infection/Immunity
Associate Professor, Biosciences
Adjunct Associate Professor
Institute for Behavioral Medicine Research, Wexner Medical Center
Center for Microbial Pathogenesis
700 Children's Drive, W410
Columbus, OH 43026
General Research: Studies in Dr. Bailey's laboratory focus on determining the impact that the intestinal microbiota have on the local mucosal immune system, and on immune reactivity at systemic sites, particularly during periods of psychological stress. In past studies, they have shown that exposure to different types of psychological stressors change the community structure of microbiota in the intestines. Their goal now is to demonstrate that these changes have significant effects on the health of the host.
Impact of Microbiota on Mucosal Immunity: The inflammatory bowel diseases involve disrupted homeostatic interactions between the microbiota and the mucosal immune system. It is well recognized that symptom severity is worsened during periods of psychological stress, but whether the stress response is involved in these disrupted homeostatic interactions is not known. They have been studying Citrobacter rodentium infection in mice because the colonic inflammation resembles components of human inflammatory bowel disease. In their studies, exposing mice to an experimental stressor during oral challenge with C. rodentium significantly increases the pathogen-induced colitis. Their preliminary studies indicate that the stressor-induced increase in colitis is dependent upon stressor-induced alterations of the microbiota, thus demonstrating a link between stress, alterations in the microbiota, and exacerbation of colonic inflammation. Current studies are focused on further characterizing the colonic inflammation, including determining the impact of the stress response on colonic epithelial cells and lamina propria leukocytes. Studies are also focused on determining which members of the microbiota contribute to the enhanced colonic inflammation.
Impact of Microbiota on Systemic Immunity: The stress response is often thought of as suppressing immune activity. However, there is accumulating evidence that in addition to suppressing immune function, the stress response can also enhance immune activity. And, although many of the mechanisms by which the stress response suppresses immunity are known, such as by the action of stress-responsive glucocorticoid hormones, the mechanisms by which the stress response enhances immune activity are not well understood. They have been using a murine social stressor, called social disruption, to study how stressor exposure enhances the ability of splenic macrophages to kill a target microbe, namely Escherichia coli. Their data indicate that stressor exposure increases the splenic macrophage oxidative burst, resulting in increased production of superoxide, and increases iNOS gene expression, resulting in increased production of nitric oxide. This increased activity ultimately results in the production of the highly microbicidal compound, peroxynitrite. Their current studies are focused on determining how the stress response enhances macrophage peroxynitrite production, and indicate that the intestinal microbiota are involved. Their goal is to determine how the microbiota can enhance splenic macrophage activity during stressor exposure.
A.R. Mackos, T.D. Eubank, N.M. Parry, M.T. Bailey. (2013). Probiotic Lactobacillus reuteri attenuates the stressor-enhanced severity of Citrobacter rodentium infection. Infection and Immunity. 81(9):3253-63.
R.G. Allen, W. P. Lafuse, N.D. Powell, J.I. Webster Marketon, L.M. Stiner-Jones, J.F. Sheridan, M.T. B ailey. (2012). Stressor-induced increase in microbicidal activity of splenic macrophages is dependent upon peroxynitrite production. Infection and Immunity. 80(10):3429-3437.
M.L. Hanke, N.D. Powell, L.M. Stiner, M.T. Bailey, and J.F. Sheridan. (2012). Beta adrenergic blockade decreases the immunomodulatory effects of social disruption stress. Brain, Behavior, and Immunity. 26(7): 1150–1159. (Journal Impact Factor: 5.06).
M.T. Bailey. (2012). The contributing role of intestinal microbiota in stressor-induced increases in susceptibility to enteric infection and systemic immunity. Hormones and Behavior. 62(3): 286-294.
R.G. Allen, W.P. Lafuse, J.D. Galley, M.M Ali, B.M.M. Ahmer, and M.T. Bailey. (2012). The intestinal microbiota are necessary for stressor-induced enhancement of splenic macrophage microbicidal activity. Brain, Behavior, and Immunity. 26(3): 371-382.
M.T. Bailey, S. E. Dowd, J.D. Galley, A.R. Hufnagle, R.G. Allen, and M. Lyte (2011). Exposure to a social stressor alters the structure of the intestinal microbiota: Implications for stressor-induced immunomodulation. Brain, Behavior, and Immunity. 25(3): 397-407.
M.T. Bailey, S.E. Dowd, N.M.A. Parry, J.D. Galley, D.B. Schauer, and M. Lyte. (2010). Stressor exposure disrupts commensal microbial populations in the intestines and leads to increased colonization by Citrobacter rodentium. Infection and Immunity. 78(4): 1509-1519.
M.T. Bailey, Kierstein, S., Spaits, M., Kinsey, S.G., Sheridan, J.F., Panettieri, R.A., and Haczku, A. (2009). Social stress enhances allergen-induced airway inflammation in mice. Journal of Immunology. 182(12): 7888–7896.
M. T. Bailey, Engler, H., Powell, N.D., Padgett, D.A., and J. F. Sheridan. (2007). Repeated social defeat increases the bactericidal activity of splenic macrophages through a toll-like receptor dependent pathway. American Journal of Physiology; Regulatory, Integrative, and Comparative Physiology; 293(3):R1180-90.
M. T. Bailey and C. L. Coe (2002) Microbial patterns of the small and large bowels in rhesus monkeys (Macaca mulatta) and the common marmoset (Callithrix jacchus). Comparative Biochemistry and Physiology. Part A. Molecular and Integrated Physiology; 133:379-388.
M. T. Bailey and C. L. Coe (2002) Endometriosis is associated with an altered profile of intestinal microflora in female rhesus monkeys. Human Reproduction; 17:1704-1708.
M. T. Bailey and C. L. Coe (1999) Maternal separation disrupts the integrity of the intestinal microflora in infant rhesus monkeys. Developmental Psychobiology; 35: 146-155.
Rebecca Allen: Rebecca is a graduate student in the Integrated Biomedical Sciences Graduate Program (IBGP) at The Ohio State University. Rebecca’s studies involve testing how a mouse stressor, called social disruption, enhances the inflammatory response during microbial challenge. Although stress is often thought to only be immunosuppressive, under certain circumstances, stress can also enhance aspects of immune reactivity, such as inflammation. Inflammation, though, must be tightly regulated, i.e., too little inflammation and too much inflammation can both have adverse effects during infection. As a result, studying how stress influences the inflammatory response will have a tremendous influence in our overall understanding of how stressor can affect health. Currently, Rebecca is studying the cellular mechanisms through which SDR enhances splenic macrophage reactivity to bacterial stimuli.
Jeffrey Galley: Jeffrey received a Bachelors of Science from The Ohio State University, majoring in Biology with an emphasis on Microbiology. After graduation, he worked for the Ohio Departments of Health and Agriculture as a Microbiologist before coming to work for Dr. Michael Bailey, drawn by the opportunity to work in immunology while considering graduate school as a future goal. He is currently working as a Research Assistant in the laboratory and is in charge of the day-to-day operations in the laboratory. In addition to these duties, Jeffrey conducts studies on the impact of stress on the indigenous microbiota. The intestines are colonized by an enormous array of commensal bacteria, known as the microbiota, that provide an important protective barrier to gastrointestinal pathogens; disrupting the microbiota has been shown to result in increased susceptibility to intestinal diseases. Because stresssors can disrupt the stability of the microbiota, he has been studying whether these stress-induced changes in microbial populations in the intestines of mice enhances their susceptibility to Citrobacter rodentium infection. These studies have identified an additional way through which exposure to stressors can influence susceptibility to infectious diseases.
Summer Research Program Dental Students:
MS: Minnesota State University Mankato
PhD: University of Wisconsin
- 2008 - present Physiology and Behavior (15 manuscripts)
- 2009 - present World Journal of Gastrointestinal Pathophysiology
- 2010 - present Gastroenterology (2 manuscripts)
- 2010 - present World Journal of Gastroenterology (2 manuscripts)
- 2010 - present International Journal of Neuropharmacology (2 manuscripts)
- 2010 - present World Journal of Gastrointestinal Pathophysiology
- 2011 - present ISRN Inflammation
- 2011 - present World Journal of Gastrointestinal Pathophysiology (2 manuscripts)
- 2012 - present Nature Reviews Neuroscience
- 2012 - present BMC Physiology
- 2012 - present Frontiers in Molecular Immunology
- 2012 - present Future Medicine
Honors/News: 2012 Robert Ader New Investigator Award, PsychoNeuroImmunology Research Society.
- 2007 - present Danone, UK
- 2009 - present Consulting. Pfizer Animal Health. Chicago
- 2009 Israeli Science Foundation. Israeli Science Foundation
- 2009 - 2010 National Science Foundation. National Science Foundation