Dr. Kannan's laboratory studies the pathogenesis of two small bacterial pathogens, Mycoplasma pneumoniae and Mycoplasma genitalium.
Despite their very small genomes these mycoplasmas are successful pathogens of human. M. pneumoniae is a frequent cause of community-acquired respiratory infections in children and adults. M. genitalium is an emerging important causative agent of sexually transmitted infections. Because of the lack of effective therapeutics and vaccines, mycoplasma diseases continue to be a significant problem for public health.
Recent outbreaks and epidemiological studies with the high incidence of mycoplasma diseases indicate the urgent need to develop new approaches for prevention and therapy. Development of such reagents, however, requires a solid understanding of the molecular biology of mycoplasma infections. They use a multidisciplinary approach involving bacterial genetics, biochemistry, cell biology as well as immunology to define the molecular interactions that occur between pathogenic mycoplasmas and their hosts.
Despite their very small genomes Mycoplasmas have developed unique ways to interact with their hosts. During their co-evolutionary balance mycoplasmas have evolved an array of virulence factors well suited to counteract a variety of host-cell responses in order to invade, survive and replicate within their hosts. They are interested in identifying and characterizing the bacterial determinants involved in these interactions as well as the molecular, cellular and immunobiology of this process.
Specific areas of interest include:
- Study the mechanism of pathogenesis of M. pneumonia through "Community acquired respiratory distress syndrome (CARDS) toxin," a toxin exclusively produced by M. pneumoniae that we identified.
- Study the mechanisms by which M.genitalium adheres, internalizes and survives within host cells. In particular, we are interested in understanding how this bacterium exploits host-cell machinery to gain access to the cell, deviating from standard pathways and reach the nucleus.
A. Becker, T.R. Kannan, A.B. Taylor, O.N. Pakhomova, Y. Zhang, J. Jiang, S.R.
Somarajan, A. Galaleldeen, S.P. Holloway, B. Demeler, J.B. Baseman and P.J.
Hart. 2015. Structure of CARDS toxin, a unique ADP-ribosylating and vacuolating
cytotoxin from Mycoplasma pneumoniae. Proc. Natl. Acad. Sci. 112 (16): 5165–70
S. Bose, J.A. Segovia, S.R.
Somarajan, T-H Chang, T.R. Kannan, and J.B. Baseman. 2014.
ADP-ribosylation of NLRP3 by Mycoplasma
pneumoniae CARDS toxin regulates inflammasome activity. mBio 23;5(6):
S.R. Somarajan, F. Al-Asadi, K.
Ramasamy, L. Pandranki, J.B. Baseman and T.R.
Kannan. 2014. Annexin A2 mediates Mycoplasma
pneumoniae CARDS toxin binding to eukaryotic cells. mBio 5(4):e01497-1514.
J. Medina, J.J. Coalson, E.G.
Brooks, C.J. LeSaux, V.T. Winter, A. Chaparro, M.F.R. Principe, L. Solis, T.R. Kannan, J.B. Baseman and P. Dube.
2014. Mycoplasma pneumoniae CARDS
toxin exacerbates ovalbumin-induced asthma-like inflammation in BALB/c mice.
PLoS One 9(7):e102613.
T.R. Kannan, M. Krishnan, R. K. Ramasamy, A. Becker,
O.N. Pakhomova, P.J. Hart, and J.B. Baseman. 2014. Functional mapping of
community acquired respiratory distress syndrome (CARDS) toxin of Mycoplasma pneumoniae defines regions
with ADP-ribosyltransferase, vacuolating, and receptor-binding activities. Mol.