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Helicobacter pylori--a seasoned pathogen by any other name.

Ahmed N, Tenguria S, Nandanwar N - Gut Pathog (2009)

Bottom Line: Several protective effects of H. pylori colonization have been considered as evidence of a presumed symbiotic relationship.The H. pylori genomes sequenced to date portray fairly high abundance of such laterally acquired genes which have no assigned functions but could be linked to inflammatory responses or other pathogenic attributes.Therefore, the powerful virulence properties and survival strategies of Helicobacter make it a seasoned pathogen; thus the efforts to portray it as a commensal or a (harmless) 'bacterial parasite' need rethinking.

View Article: PubMed Central - HTML - PubMed

Affiliation: Pathogen Biology Laboratory, Department of Biotechnology, School of Life Sciences, University of Hyderabad, Hyderabad, India. niyazsl@uohyd.ernet.in

ABSTRACT
Helicobacter pylori is a well known inhabitant of human stomach which is linked to peptic ulcer disease and gastric adenocarcinoma. It was recently shown in several studies that H. pylori can be harnessed as a surrogate marker of human migration and that its population structure and stratification patterns exactly juxtapose to those of Homo sapiens. This is enough a testimony to convey that H. pylori may have coevolved with their host. Several protective effects of H. pylori colonization have been considered as evidence of a presumed symbiotic relationship. Contrary to this assumption is the presence of a strong virulence apparatus within H. pylori; why a co-evolved parasite would try inflicting its host with serious infection and even causing cancer? The answer is perhaps embedded in the evolutionary history of both the bacterium and the host. We discuss a hypothetical scenario wherein H. pylori may have acquired virulence genes from donors within its environment that varied with change in human history and ecology. The H. pylori genomes sequenced to date portray fairly high abundance of such laterally acquired genes which have no assigned functions but could be linked to inflammatory responses or other pathogenic attributes. Therefore, the powerful virulence properties and survival strategies of Helicobacter make it a seasoned pathogen; thus the efforts to portray it as a commensal or a (harmless) 'bacterial parasite' need rethinking.

No MeSH data available.


Related in: MedlinePlus

Genome evolution, global diversification and spread of H. pylori (sub-) populations. Horizontal gene transfer and genome plasticity likely contributed to the evolution of pathogenic variants from non-pathogenic colonizers. Modern H. pylori populations thus derived their gene pools from ancestral populations that arose on different continents and can be correlated with different migrations of human populations and other Neolithic events such as arrival of agriculture. The beginning of agriculture and the domestication of farm animals (which seem to have occurred hand in hand but across multiple domestication events in a continent specific manner) suggest a scenario, as depicted here, which can be linked to the acquisition of virulence by H. pylori. It can be hypothesized that early bacterial communities originating from crop plants, animals or rodent pests etc. rampant in the vicinity of early human societies may have served as donors of some of the virulence gene cassettes. Such genetic elements may have been acquired by H. pylori either bit by bit or en-bloc, at some point of time, through horizontal gene transfer events. There are indirect evidences to this effect in the form of sequence and structural similarities of some of the H. pylori's virulence genes to their homologues in plant pathogens and environmental bacteria. Also, we believe that the extraneous virulence genes may have conferred some survival advantage upon H. pylori making them fitter in different human and animal hosts and, as a result, the pathogen may have spread selectively in a geographically compartmentalized manner.
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Figure 1: Genome evolution, global diversification and spread of H. pylori (sub-) populations. Horizontal gene transfer and genome plasticity likely contributed to the evolution of pathogenic variants from non-pathogenic colonizers. Modern H. pylori populations thus derived their gene pools from ancestral populations that arose on different continents and can be correlated with different migrations of human populations and other Neolithic events such as arrival of agriculture. The beginning of agriculture and the domestication of farm animals (which seem to have occurred hand in hand but across multiple domestication events in a continent specific manner) suggest a scenario, as depicted here, which can be linked to the acquisition of virulence by H. pylori. It can be hypothesized that early bacterial communities originating from crop plants, animals or rodent pests etc. rampant in the vicinity of early human societies may have served as donors of some of the virulence gene cassettes. Such genetic elements may have been acquired by H. pylori either bit by bit or en-bloc, at some point of time, through horizontal gene transfer events. There are indirect evidences to this effect in the form of sequence and structural similarities of some of the H. pylori's virulence genes to their homologues in plant pathogens and environmental bacteria. Also, we believe that the extraneous virulence genes may have conferred some survival advantage upon H. pylori making them fitter in different human and animal hosts and, as a result, the pathogen may have spread selectively in a geographically compartmentalized manner.

Mentions: The acquisition of the cag pathogenicity island (PAI) has therefore been the subject of debate on its origin and circumstances under which the PAI was imported from a foreign source [16]. Taking into account the comprehensive genetic analyses that have been performed, it is possible to predict a possible evolutionary scenario (Fig. 1) that supports the proposition that the cagPAI was acquired by ancestral H. pylori populations that arose on different continents before agriculture began in the civilized world. The acquisition of the PAIs might have occurred in H. pylori populations quite recently, possibly due to close contact of humans with domesticated animals, crops or rodent pests surrounding them. Such an inter species gene transfer could be explained partly based on the fact that many constituent genes of the cagPAI reveal well-established homologies to the type IV systems of Agrobacterium tumifaciens [18] and that cagA-like sequences have been reported from some Aeromonas isolates [19], obtained from environmental samples. Subsequent environmental changes and evolution of the food habits might have led to further continent specific adaptation of H. pylori. To date, the genetic structure of H. pylori is highly geographically oriented, both with respect to the core and the flexible genome components.


Helicobacter pylori--a seasoned pathogen by any other name.

Ahmed N, Tenguria S, Nandanwar N - Gut Pathog (2009)

Genome evolution, global diversification and spread of H. pylori (sub-) populations. Horizontal gene transfer and genome plasticity likely contributed to the evolution of pathogenic variants from non-pathogenic colonizers. Modern H. pylori populations thus derived their gene pools from ancestral populations that arose on different continents and can be correlated with different migrations of human populations and other Neolithic events such as arrival of agriculture. The beginning of agriculture and the domestication of farm animals (which seem to have occurred hand in hand but across multiple domestication events in a continent specific manner) suggest a scenario, as depicted here, which can be linked to the acquisition of virulence by H. pylori. It can be hypothesized that early bacterial communities originating from crop plants, animals or rodent pests etc. rampant in the vicinity of early human societies may have served as donors of some of the virulence gene cassettes. Such genetic elements may have been acquired by H. pylori either bit by bit or en-bloc, at some point of time, through horizontal gene transfer events. There are indirect evidences to this effect in the form of sequence and structural similarities of some of the H. pylori's virulence genes to their homologues in plant pathogens and environmental bacteria. Also, we believe that the extraneous virulence genes may have conferred some survival advantage upon H. pylori making them fitter in different human and animal hosts and, as a result, the pathogen may have spread selectively in a geographically compartmentalized manner.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2806874&req=5

Figure 1: Genome evolution, global diversification and spread of H. pylori (sub-) populations. Horizontal gene transfer and genome plasticity likely contributed to the evolution of pathogenic variants from non-pathogenic colonizers. Modern H. pylori populations thus derived their gene pools from ancestral populations that arose on different continents and can be correlated with different migrations of human populations and other Neolithic events such as arrival of agriculture. The beginning of agriculture and the domestication of farm animals (which seem to have occurred hand in hand but across multiple domestication events in a continent specific manner) suggest a scenario, as depicted here, which can be linked to the acquisition of virulence by H. pylori. It can be hypothesized that early bacterial communities originating from crop plants, animals or rodent pests etc. rampant in the vicinity of early human societies may have served as donors of some of the virulence gene cassettes. Such genetic elements may have been acquired by H. pylori either bit by bit or en-bloc, at some point of time, through horizontal gene transfer events. There are indirect evidences to this effect in the form of sequence and structural similarities of some of the H. pylori's virulence genes to their homologues in plant pathogens and environmental bacteria. Also, we believe that the extraneous virulence genes may have conferred some survival advantage upon H. pylori making them fitter in different human and animal hosts and, as a result, the pathogen may have spread selectively in a geographically compartmentalized manner.
Mentions: The acquisition of the cag pathogenicity island (PAI) has therefore been the subject of debate on its origin and circumstances under which the PAI was imported from a foreign source [16]. Taking into account the comprehensive genetic analyses that have been performed, it is possible to predict a possible evolutionary scenario (Fig. 1) that supports the proposition that the cagPAI was acquired by ancestral H. pylori populations that arose on different continents before agriculture began in the civilized world. The acquisition of the PAIs might have occurred in H. pylori populations quite recently, possibly due to close contact of humans with domesticated animals, crops or rodent pests surrounding them. Such an inter species gene transfer could be explained partly based on the fact that many constituent genes of the cagPAI reveal well-established homologies to the type IV systems of Agrobacterium tumifaciens [18] and that cagA-like sequences have been reported from some Aeromonas isolates [19], obtained from environmental samples. Subsequent environmental changes and evolution of the food habits might have led to further continent specific adaptation of H. pylori. To date, the genetic structure of H. pylori is highly geographically oriented, both with respect to the core and the flexible genome components.

Bottom Line: Several protective effects of H. pylori colonization have been considered as evidence of a presumed symbiotic relationship.The H. pylori genomes sequenced to date portray fairly high abundance of such laterally acquired genes which have no assigned functions but could be linked to inflammatory responses or other pathogenic attributes.Therefore, the powerful virulence properties and survival strategies of Helicobacter make it a seasoned pathogen; thus the efforts to portray it as a commensal or a (harmless) 'bacterial parasite' need rethinking.

View Article: PubMed Central - HTML - PubMed

Affiliation: Pathogen Biology Laboratory, Department of Biotechnology, School of Life Sciences, University of Hyderabad, Hyderabad, India. niyazsl@uohyd.ernet.in

ABSTRACT
Helicobacter pylori is a well known inhabitant of human stomach which is linked to peptic ulcer disease and gastric adenocarcinoma. It was recently shown in several studies that H. pylori can be harnessed as a surrogate marker of human migration and that its population structure and stratification patterns exactly juxtapose to those of Homo sapiens. This is enough a testimony to convey that H. pylori may have coevolved with their host. Several protective effects of H. pylori colonization have been considered as evidence of a presumed symbiotic relationship. Contrary to this assumption is the presence of a strong virulence apparatus within H. pylori; why a co-evolved parasite would try inflicting its host with serious infection and even causing cancer? The answer is perhaps embedded in the evolutionary history of both the bacterium and the host. We discuss a hypothetical scenario wherein H. pylori may have acquired virulence genes from donors within its environment that varied with change in human history and ecology. The H. pylori genomes sequenced to date portray fairly high abundance of such laterally acquired genes which have no assigned functions but could be linked to inflammatory responses or other pathogenic attributes. Therefore, the powerful virulence properties and survival strategies of Helicobacter make it a seasoned pathogen; thus the efforts to portray it as a commensal or a (harmless) 'bacterial parasite' need rethinking.

No MeSH data available.


Related in: MedlinePlus