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Mitchell Balish
Assistant Chair of Microbiology and Professor
Cell, Molecular and Structural Biology Graduate Program, Microbiology

Mitchell F. Balish

Contact Info

(513) 529-0167
64 Pearson Hall

Education

Ph.D. Biochemistry and Molecular Biology, Emory University (1998)

Research Interests

Mycoplasmas are a group of bacteria, often pathogenic, with some very unusual features compared to other bacteria. For one, they are bounded only by a single membrane and no cell wall, a trait that they share with animal cells but with few other kinds of cells among the vast array of organisms in the world. Second, although they are not physically the smallest cells, most mycoplasma species are at least 10 times smaller than model bacteria like E. coli, presenting special challenges for their study. Finally, mycoplasmas have the smallest genomes among organisms that can be cultured independently of other cells, causing them to rely on host cells to provide most nutrients in nature, while also making them minimalistic models for researchers aiming to understand the fundamental properties of all living cells.

In the Balish Mycoplasmology Lab, graduate and undergraduate 黑料社区s perform experiments to ask significant questions about mycoplasmas, usually focusing on species that are either frank or opportunistic pathogens of humans. It is important to study these organisms because many of them are highly prevalent, the infections they cause are long-lasting, there are no vaccines available, and antibiotic resistance is rising and is dangerously high in some parts of the world. Understanding what mycoplasmas do during infection and disease, and ultimately how they do these things, could provide critical information that leads to the development of new therapeutic agents that will improve the lives of millions of people each year who suffer from chronic infection with mycoplasmas. The important work carried out by our 黑料社区s, involving a diverse array of cell biological, molecular biological, and biochemical techniques, falls into several overlapping areas.

1. Structural features of mycoplasma cells.

Some important species that infect humans, like the respiratory pathogen Mycoplasma pneumoniae and the sexually transmitted pathogens Mycoplasma genitalium and Mycoplasma penetrans, rely on prominent polar protrusions called attachment organelles for adherence to the host cells and movement along surfaces. These structures are undergirded by novel cytoskeletal proteins that are found only in mycoplasmas, frustrating efforts to understand these proteins through comparison with model organisms. Furthermore, and even more remarkably, different groups of mycoplasmas use entirely different proteins to create these structures, and they use fundamentally different mechanisms to power motility, suggesting convergent evolution of attachment organelles. Some 黑料社区 projects are aimed at how the components of attachment organelles specifically function in the architecture, motility, and virulence-related properties of these structures.

2. Regulation of mycoplasma virulence factor production.

Biofilms are aggregates of single-celled organisms that occur naturally and confer protection from host defenses, antibiotics, and fluctuations in environmental conditions. When M. pneumoniae cells form biofilm structures, which we suspect are important in chronic disease caused by this organism, they reduce production of several molecules associated with virulence, including hydrogen peroxide, hydrogen sulfide, and the ADP-ribosylating CARDS toxin. The mechanisms by which M. pneumoniae carries out this regulation is entirely unknown. Some 黑料社区 projects are focused on testing hypotheses about the mechanism of virulence factor regulation, and others are aimed at understanding biofilm formation in M. pneumoniae and other mycoplasma species.

3. Interactions between mycoplasmas and host cells.

Different mycoplasma species interact with host cells in different ways. M. pneumoniae, for example, is almost certainly an exclusively extracellular pathogen, whereas M. penetrans is named for its ability to invade cells. Although important aspects of the progression and features of infection of host cells have been characterized, some important gaps in knowledge remain to be filled in. In the case of M. pneumoniae, there is little information about the impact of biofilm structures on host cells. For M. penetrans, most of the work has been done with cell types whose relevance to infection is marginal. Some 黑料社区 projects address these questions by investigating the effects of these pathogenic bacteria on appropriate host cells.

4. Cell division.

Bacteria generally utilize the process of cell wall synthesis to enable cells to divide, but mycoplasmas have no cell walls. Mycoplasmas that have attachment organelles typically use the force of motility to help separate cells. But most mycoplasma species, including a large number of important pathogens of animals and humans, do not have attachment organelles, leaving their mechanism for cell division a mystery. These bacteria undergo an array of changes in shape and organization during the process of division, but these changes are not well-characterized. Some 黑料社区 projects aim to understand the sequence of events and the processes that occur during cell division of mycoplasmas that lack attachment organelles.

Selected Publications

Peer-Reviewed Research Articles

  • Fahim, R.A.*, Z.E.D. Rodriguez*, Z. Oestreicher, N.R. Schwab*, N.E. Young**, K. Shrestha*, and M.F. Balish. 2025. Eradication of Mycoplasma pneumoniae biofilm towers by treatment with hydrogen peroxide or antibiotic combinations acting synergistically. PLoS ONE 20:e0329571
  • Schwab, N.R.*, N.E. Young**,  D.U. Nzenwata*, E. Toh, J.A. Mikulin**, T.J. Wilson, D.E. Nelson, and M.F. Balish. 2023. Characterization of virulence-associated traits in Mycoplasma penetrans strains acting as likely etiological agents of idiopathic nongonococcal urethritis. J. Infect. Dis. 227:1050-1058.
  • Feng, M.*, A.C. Burgess**, R.R. Cuellar**, N.R. Schwab*, and M.F. Balish. 2021. Modeling persistent Mycoplasma pneumoniae biofilm infections in a submerged BEAS-2B bronchial epithelial tissue culture model. J. Med. Microbiol. 70:001266.
  • Feng, M.*, A.C. Schaff**, and M.F. Balish. 2020. Mycoplasma pneumoniae biofilms grown in vitro: traits associated with persistence and cytotoxicity. Microbiology 166:629-640.
  • Feng, M.*, A.C. Schaff**, S.A. Cuadra Aruguete**, H.E. Riggs*, S.L. Distelhorst*, and M.F. Balish. 2018. Development of Mycoplasma pneumoniae biofilms in vitro and the limited role of motility. Int. J. Med. Microbiol. 308:324-334.
  • Distelhorst, S.L.*, D.A. Jurkovic*, J. Shi, G.J. Jensen, and M.F. Balish. 2017. The variable internal structure of the Mycoplasma penetrans attachment organelle revealed by biochemical and microscopic analyses: implications for attachment organelle mechanism and evolution. J. Bacteriol. 199:e00069-17.
  • Pritchard, R.E.*, and M.F. Balish. 2015. Mycoplasma iowae: relationships among oxygen, virulence, and protection from oxidative stress. Vet. Res. 46:36.
  • Pritchard, R.E.*, A.J. Prassinos**, J.D. Osborne, Z. Raviv, and M.F. Balish. 2014. Reduction of hydrogen peroxide accumulation and toxicity by a catalase from Mycoplasma iowae. PLoS ONE 9:e105188.
  • Jurkovic, D.A.*, M.R. Hughes, and M.F. Balish. 2013. Analysis of energy sources for Mycoplasma penetrans gliding motility. FEMS Microbiol. Lett. 338:39-45.
  • Jurkovic, D.A.*, J.T. Newman**, and M.F. Balish. 2012. Conserved terminal organelle morphology in Mycoplasma penetrans and Mycoplasma iowae. J. Bacteriol. 194:2877-2883.
  • Relich, R.F.*, and M.F. Balish. 2011. Insights into the function of Mycoplasma pneumoniae protein P30 from orthologous gene replacement. Microbiology 157:2862-2870.
  • Relich, R.F.*, A.J. Friedberg**, and M.F. Balish. 2009. Novel cellular organization in a gliding mycoplasma, Mycoplasma insons. J. Bacteriol. 191:5312-5314.
  • Hatchel, J.M.*, and M.F. Balish. 2008. Attachment organelle ultrastructure correlates with phylogeny, not gliding motility properties, in Mycoplasma pneumoniae relatives. Microbiology 154:286-295.
  • Hatchel, J.M.*, R.S. Balish, M.L. Duley, and M.F. Balish. 2006. Ultrastructure and gliding motility of Mycoplasma amphoriforme, a possible human respiratory pathogen. Microbiology 152:2181-2189.

Review Articles

  • Waites, K.B., L. Xiao, Y. Liu, M.F. Balish, and T.P. Atkinson. 2017. Mycoplasma pneumoniae from the respiratory tract and beyond. Clin. Microbiol. Rev. 30:747-809.
  • Balish, M.F., and S.L. Distelhorst*. 2016. Potential molecular targets for narrow-spectrum agents to combat Mycoplasma pneumoniae infection and disease. Front. Microbiol. 7:205.
  • Balish, M.F. 2014. Mycoplasma pneumoniae, an underutilized model for bacterial cell biology. J. Bacteriol. 196:3675-3682.
  • Atkinson, T.P., M.F. Balish, and K.B. Waites. 2008. Epidemiology, clinical manifestations, pathogenesis and laboratory detection of Mycoplasma pneumoniae infections. FEMS Microbiol. Rev. 32:956-973.
  • Balish, M.F., and D.C. Krause. 2006. Mycoplasmas:  a distinct cytoskeleton for wall-less bacteria. J. Mol. Microbiol. Biotechnol. 11:244-255.
  • Balish, M.F. 2006. Subcellular structures of mycoplasmas. Front. Biosci. 11:2017-2027.
*: graduate 黑料社区
**: undergraduate researcher