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Helicobacter pylori
Martin J. Blaser, Denise Kirschner
The equilibria that allow bacterial persistence in human hosts
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Nature, Vol 449, j18, October 2007, pp 483-489
Niyaz Ahmed, of the
Pathogen Evolution Laboratory, Centre for DNA Fingerprinting and
Diagnostics, India, gives his comments on the article at
facultyof1000.com
This is a provocative yet legitimate proposal on how pathogenic
bacteria adapt to their co-evolved hosts across a wide array of
conditions linked to biology of both the host and pathogen, over huge
evolutionary timescales. The authors focus on the concept that
persistence represents finely negotiated, well balanced host-
microbial interests, culminating in a long-term equilibrium whose
maintenance requires a series of evolved, nested equilibria leading
to the overall homeostasis. To support their assumption the authors
harness observed pathobiology of three dreaded pathogens (H. pylori,
S. typhi and M. tuberculosis). Based on the fact that genomic and
biological features of these 'specialist' bacteria are quite diverse,
authors generalize their model for other pathogens as well. If it is
so, this model may also fit to commensals and other 'generalist'
bacteria who might have accompanied humans in various capacities
throughout their association. This dogma may therefore be relevant in
understanding acquisition and/or attenuation of virulence with the
change in human history and ecology. Although this is a largely
speculative treatise, I am sure it will provide a foundation for
future experimental evidence.
Raymond Mejia, of the
National Heart, Lung and Blood Institute (NHLBI),
and the National Institutes of Health (NIH),
gives his comments on the article at
facultyof1000.com
This study uses a mathematical model to explain bacterial persistence
in a host population. Symbiosis is characterized by existence of
evolutionary stable states that permit homeostasis. The model is applied
to three bacteria with human hosts, H. pylori, S. typhi, and M. tuberculosis,
and can be utilized to investigate how virulence may vary with changes in human ecology.
Joseph, I., Kirschner, D.,
A Model for the Study of Helicobacter Pylori Interaction with Human Gastric Acid Secretion
.
Journal of Theoretical Biology 228:55-80, 2004
Sud, D., Joseph, I., Kirschner, D.,
Predicting Efficacy of Proton Pump Inhibitors in Regulating Gastric Acid Secretion
.
Journal of Biological Systems, Vol. 12, No. 1, pg 1-34, 2004
Marino, S., Ganguli, S., Joseph, I.M.P., Kirschner, D.E.,
The Importance of an Inter-compartmental Delay in a Model for Human Gastric Acid Secretion
.
Bulletin of Math. Biology, 65:963-990,2003.
Joseph, I.M., Y. Zavros, J.L. Merchant, and D. Kirschner,
A model for integrative study of human gastric acid secretion
.
J Appl Physiology 94, pg. 1602-1619, 2003.
Denise E. Kirschner, Reconstructing Microbial Pathogenesis
ASM News Vol 67, Num. 11, pp. 566-573, 2001
Kirschner D and Freter R. Mathematical Models of Persistent
Bacterial Infections. In: Nataro J, Blaser MJ, and Cunningham-Rungles
S. (eds): Persistant Bacterial Infections, for ASM Press Publications, Washington,
DC, pp. 79-99, 2000.
Falk P, Syder A, Guruge J, Kirschner D, Blaser
M and Gordon J.
Theoretical
and experimental approaches for studying factors that define the relationship
between Heliobacter pylori and its host. Trends in Microbiol
Vol 8, pps 321-329, July 2000.
Blaser MJ and Kirschner D. Dynamics of Helicobacter pylori
colonization in relation to the host immune response. PNAS,
96:8359-8364, 1999.
Kirschner D and Blaser M. The dynamics of Heliocobacter
pylori infection of the human stomach. J Theor Biol 176:281-290,
1995.
ERRATA
Marino, S., Ganguli, S., Joseph, I.M.P., Kirschner, D.E.,
The Importance of an Inter-compartmental Delay in a Model for Human Gastric Acid
Secretion
.
Bulletin of Math. Biology, 65:963-990, 2003.
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