Motility and Chemotaxis Mediate the Preferential Colonization of Gastric Injury Sites by Helicobacter pylori

Motility and Chemotaxis Mediate the Preferential Colonization of Gastric Injury Sites by Helicobacter pylori. Aihara, E., Closson, C., Matthis, A. L., Schumacher, M. A., Engevik, A. C., Zavros, Y., Ottemann, K. M., & Montrose, M. H. PLoS Pathog, 10(7):e1004275, July, 2014.

Paper doi abstract bibtex

Author Summary H. pylori is a disease-causing bacterium that commonly infects the human stomach in both developed and underdeveloped countries. Infected individuals can develop digestive diseases, including stomach inflammation, peptic ulcer, and cancer. There has been only limited investigation into the events when H. pylori first interacts with stomach tissue. Using anesthetized mice in which we have induced microscopic damage to the stomach surface, we find that H. pylori is able to rapidly detect and navigate towards this damage site. Within minutes, bacterial accumulation slows repair of the damage. This is the earliest event of H. pylori pathogenesis that has been reported in vivo. We further define that this pathology is due to the bacterial accumulation at damage sites and that this also occurs in a model of larger stomach damage (ulceration). The broader implications of our work are that even sub-clinical insults to the stomach that occur in daily life (damage from grinding of food, ingestion of alcohol, taking an aspirin) can potentially attract H. pylori and not only slow repair of any existing damage, but maybe also provide an initiation site that can start the pathogenic sequence of stomach disease caused by H. pylori.

@article{aihara_motility_2014,
	title = {Motility and {Chemotaxis} {Mediate} the {Preferential} {Colonization} of {Gastric} {Injury} {Sites} by {Helicobacter} pylori},
	volume = {10},
	url = {http://dx.doi.org/10.1371/journal.ppat.1004275},
	doi = {10.1371/journal.ppat.1004275},
	abstract = {Author Summary H. pylori is a disease-causing bacterium that commonly infects the human stomach in both developed and underdeveloped countries. Infected individuals can develop digestive diseases, including stomach inflammation, peptic ulcer, and cancer. There has been only limited investigation into the events when H. pylori first interacts with stomach tissue. Using anesthetized mice in which we have induced microscopic damage to the stomach surface, we find that H. pylori is able to rapidly detect and navigate towards this damage site. Within minutes, bacterial accumulation slows repair of the damage. This is the earliest event of H. pylori pathogenesis that has been reported in vivo. We further define that this pathology is due to the bacterial accumulation at damage sites and that this also occurs in a model of larger stomach damage (ulceration). The broader implications of our work are that even sub-clinical insults to the stomach that occur in daily life (damage from grinding of food, ingestion of alcohol, taking an aspirin) can potentially attract H. pylori and not only slow repair of any existing damage, but maybe also provide an initiation site that can start the pathogenic sequence of stomach disease caused by H. pylori.},
	number = {7},
	urldate = {2015-01-11TZ},
	journal = {PLoS Pathog},
	author = {Aihara, Eitaro and Closson, Chet and Matthis, Andrea L. and Schumacher, Michael A. and Engevik, Amy C. and Zavros, Yana and Ottemann, Karen M. and Montrose, Marshall H.},
	month = jul,
	year = {2014},
	pages = {e1004275}
}

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