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The microbes that persistently colonise their vertebrate hosts are not accidental.1 Although highly numerous and diverse, there is specificity by site and substantial conservation between individuals. The genus Helicobacter includes spiral, highly motile, urease-positive, Gram-negative bacteria that colonise the stomach in many mammals. Each mammal has one or more dominant Helicobacter species and they are highly, if not exclusively, host species-specific.2 Such observations are consistent with the hypothesis that when ancestral mammals diverged from reptiles about 150 million years ago, they contained ancestral helicobacters, which then diverged as their hosts changed. According to this hypothesis, helicobacters represent ancestral biota (flora) in the mammalian stomach. The human-adapted strain is H pylori,3 which has not been reproducibly observed in any animals other than humans and other primates.3
Although we can not reliably estimate how long H pylori has been in the human stomach, its ancestors may have been present when our humanoid ancestors diverged from other primates about four million years ago. Consistent with this view are results from phylogeographic studies; strong and consistent evidence indicates that our ancestors already were carrying gastric H pylori when a group that ultimately populated much of the world last left Africa, more than 58 000 years ago.4 In any case, H pylori has been colonising the stomach of humans since at least Paleolithic times.
In this paper, we examine the evidence concerning the relationship of this ancient member of the human microbiota, and particularly its absence, with the recent and on-going epidemic of asthma and related allergic disorders. We discuss the possibility that gastric H pylori colonisation protects against these disorders and that its disappearance has fuelled their rise.
H PYLORI ACQUISITION AND PERSISTENCE
H pylori is acquired, and may be detected, in early childhood usually after the first year of life.5 Transmission is …
Footnotes
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Competing interests: Dr Blaser, as a co-discoverer of cagA at Vanderbilt University, can receive royalties from the commercial exploitation of cagA. No diagnostic tests for cagA are currently licensed.
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Funding: This research was supported by grant ES000260 from the National Institute of Environmental Health Sciences, grant CA016087 from the National Cancer Institute, grant RO1GM63270 from the National Institutes of Health, the Diane Belfer Program in Human Microbial Ecology, the Senior Scholar Award of the Ellison Medical Foundation, Ellison Medical Foundation, and Colten Family Foundation.