University of Florida

Mary B. Brown, Ph.D.

Overall Research Interests: My laboratory is involved in defining the pathogenic mechanisms by which mycoplasmas cause both respiratory and urogenital infections. We work with a number of host species, including rodents, food and fiber animals, environmentally threatened gopher and desert tortoises, and humans. The inherent mechanisms by which mycoplasmas colonize the host and induce chronic disease are surprisingly similar, despite the wide range of hosts. Several of our key efforts are described.

Models of Intrauterine Infection: Microbial infections of the chorioamnion and amniotic fluid have devastating effects on pregnancy outcome. Genital mycoplasmosis is a naturally occurring disease of rats that makes it an excellent model to study the adverse effects of infectious agents in pregnancy as well as the immunomodulatory effects of infectious agents and their impact on reproductive function. We have demonstrated that M. pulmonis causes an ascending infection in Sprague Dawley rats that is characterized by placentitis and chorioamnionitis and results in significant fetal wastage and decreased birth weight. We have characterized the fetal immune response to infection and identified resistant and susceptible strains of rats. Using microarray analysis, we have identified genomic and proteomic differences between the resistant and susceptible strains. Most recently, we have begun collaborations with colleagues in the College of Dentistry to expand our rodent model for use with Porphyromonas gingivalis, a periodontal pathogen that has been associated with pregnancy loss.

Mycoplasmosis in food and fiber animals: Our laboratory is studying the host:pathogen interactions during mycoplasmal infections of ruminants as well as interventions to limit disease. We have established a model for otitis media and pneumonia in which we can selectively stimulate the upper or lower respiratory tract immune response. We have also been involved in field trials for potential M. bovis vaccines. Recently, we have completed the genome sequence of M. bovis F1 strain used in the experimental infection studies in calves, and will use this information for molecular epidemiology studies and for targeted pathogenesis studies. These data will provide information critical for effective vaccine strategies. In addition to the work with M. bovis, our laboratory also is investigating the role of an extracellular protease of large colony M. mycoides as a model system to understand gene regulation in mycoplasmas and host:pathogen interactions during experimental infection and systemic disease.

Urinary tract infections: We have developed an animal model for UTI with U. urealyticum and have identified resistant and susceptible strains of rats. This model is characterized by rat strains that are colonized without serious complications, rat strains that clear infection, and rats strains that develop struvite stones with marked pathology to the bladder. This model will permit us to identify potential genes involved in genetic susceptibility to both UTI and urolith formation.

Representative Publications:
Peltier, MR and MB Brown. 2005. Genital mycoplasmosis causes increased levels of mRNA for IL-6 and TNF-alpha in the placenta. Am J Reprod Immunol 53:189-198.

Edwards RK, Ferguson RJ, Reyes L, Brown M, Theriaque DW, Duff P. 2006. Assessing the relationship between preterm delivery and various microorganisms recovered from the lower genital tract. J Matern Fetal Neonatal Med 19 (6):357-363.

Oli MK, Venkataraman M, Klein PA, Wendland LD, Brown, MB. 2006. Population dynamics of infectious diseases: a discrete time model. Ecol Model. 198:183-194.

Reyes L, Reinhard M, O’Donell LJ, Stevens J, Brown MB. 2006 Rat strains differ in susceptibility to Ureaplasma induced UTI and struvite stone formation. Infect Immun. 74:6656-6664.

Peltier MR, Barney BM, Brown MB. 2007 Effect of experimental genital mycoplasmosis on production of matrix metalloproteinases in membranes and amniotic fluid of Sprague-Dawley rats. Am J Reprod Immunol 57:116-121.

Wendland LD, Zacher LA, Klein PA, Brown DR, Demcovitz D, Littell R, and Brown MB. 2007. An improved ELISA for Mycoplasma agassizii exposure: A valuable tool in the management of environmentally sensitive tortoise populations. Clin Vacc Immunol. 14:1190-1195.

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Mary B Brown, Ph.D.
Professor
Department of Infectious Diseases and Pathology
Ph.D., University of Alabama at Birmingham

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