C61: Motility and Toxic Molecule Production as Potential Virulence Factors of the Human Opportunistic Pathogen Mycoplasma amphoriforme

Mycoplasma amphoriforme is a species of bacteria that is likely a human opportunistic pathogen contributing to respiratory tract infections (1). M. amphoriforme was first isolated in 1999, formally described in a patient in 2003 (1), and the first case of this species in the Western hemisphere was recently isolated (Xiao, unpublished). Accordingly, its full role as a human pathogen has yet to be elucidated. There are several common factors across many species of mycoplasmas that play a role in their pathogenicity, such as a polar protrusion or attachment organelle, gliding motility, and the production of toxic molecules (2,3). The well-established human pathogen, Mycoplasma pneumoniae, produces H2O2 (hydrogen peroxide) as a by-product of its metabolism (2) that can damage host cell DNA (5). M. pneumoniae also produces H2S (hydrogen sulfide), which works in conjunction with H2O2 to cause damage to red blood cells (6). In addition to its role in host cell adherence, the attachment organelle of M. pneumoniae demonstrates gliding motility in the direction of this structure (4). M. amphoriforme shares many similarities with M. pneumoniae, and it is therefore hypothesized that toxic molecule production and motility may also be important to the virulence of M. amphoriforme. The purpose of this study is to further characterize M. amphoriforme in terms of its motility to quantify its average speed as well as production of the toxic molecules H2O2 and H2S which may contribute to their virulence in the host cell. In addition, immunofluorescence microscopy studies will enable determination of the efficacy of an antibody allowing for detection of this organism in a future tissue culture model. Insights into toxic molecule production and motility of M. amphoriforme will aid in future studies of virulence traits of this organism and could point toward the development of treatments to help infected patients.

References:

  1. Webster D, Windsor H, Ling C, Windsor D, Pitcher D. 2003. Chronic Bronchitis in Immunocompromised Patients: Association with a Novel Mycoplasma Species. Eur J Clin Microbiol Infect Dis 22: 530–534.

  2. Hames C, Halbedel S, Hoppert M, Frey J, Stulke J. 2009. Glycerol metabolism is important for cytotoxicity in Mycoplasma pneumoniae. J Bacteriol. 191(3): 747-753.

  3. Balish M. 2014. Mycoplasma pneumoniae, an underutilized model for bacterial cell biology. J. Bacteriol. 196:3675-3682.

  4. Szczepanek SM, Majumder S, Sheppard ES, Liao X, Rood D, Tulman ER, Wyand S, Krause DC, Silbart LK, Geary SJ. 2012. Vaccination of BALB/c mice with an avirulent Mycoplasma pneumoniae P30 mutant results in disease exacerbation upon challenge with a virulent strain. Infect. Immun. 80:1007-1014.

  5. Sun G, Xu X, Wang Y, Shen X, Chen Z, Yang J. 2008. Mycoplasma pneumoniae infection induces reactive oxygen species and DNA damage in A549 human lung carcinoma cells. Infect Immun. 76:4403-4413.

  6. Großhennig S, Ischebeck T, Gibhardt J, Busse J, Fuessner I, Stülke J. 2016. Hydrogen sulfide is a novel potential virulence factor of Mycoplasma pneumoniae: characterization of the unusual cysteine desulfurase/desulfhydrase HapE. Mol Microbiol. 100: 43-54. PMID: 26711628

Author: Rachel R. Cuellar

Faculty Advisor: Mitchell F. Balish, Department of Microbiology

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