Document Detail


Helicobacter pylori requires TlpD-driven chemotaxis to proliferate in the antrum.
MedLine Citation:
PMID:  22802346     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Different disease outcomes of Helicobacter pylori infection correlate with distinct inflammation patterns. These different inflammatory distributions may be initiated by differences in bacterial localization. One H. pylori property known to affect murine stomach localization is chemotaxis, the ability to move in response to chemical cues. In this report, we used nonchemotactic mutants (Che(-)) to analyze whether chemotaxis is required for initial colonization of particular stomach regions or for subsequent growth therein. We found that H. pylori behaves differently in the corpus, antrum, and corpus-antrum transition zone subregions of the stomach. This outcome suggests that these regions contain unique chemotactic signals. In the corpus, H. pylori utilizes chemotaxis for initial localization but not for subsequent growth. In contrast, in the antrum and the corpus-antrum transition zone, chemotaxis does not help initial colonization but does promote subsequent proliferation. To determine which chemoreceptor is responsible for the corpus-antrum phenotypes, we infected mice with strains lacking each chemoreceptor. Strains lacking TlpA, TlpB, or TlpC displayed only modest deviations from the wild-type phenotype, while strains lacking TlpD resembled the Che(-) mutant in their antral colonization defect and fared even worse than the Che(-) mutant in the corpus. Additional analysis showed that inflammation is worse in the antrum than in the corpus in both wild-type and Che(-) mutant infections. These results suggest that chemotaxis, specifically, that controlled by TlpD, is necessary for H. pylori to survive or grow in the environment of increased inflammation in the antrum.
Authors:
Annah S Rolig; James Shanks; J Elliot Carter; Karen M Ottemann
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-07-16
Journal Detail:
Title:  Infection and immunity     Volume:  80     ISSN:  1098-5522     ISO Abbreviation:  Infect. Immun.     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-09-12     Completed Date:  2012-12-03     Revised Date:  2013-07-12    
Medline Journal Info:
Nlm Unique ID:  0246127     Medline TA:  Infect Immun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3713-20     Citation Subset:  IM    
Affiliation:
Department of Molecular, Cellular, and Developmental Biology, University of California, Santa Cruz, Santa Cruz, California, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Bacterial Proteins / genetics,  metabolism*
Chemotaxis / physiology
Epithelium / microbiology,  physiology
Female
Helicobacter Infections / microbiology*,  pathology
Helicobacter pylori / genetics,  metabolism*
Mice
Mice, Inbred C57BL
Mutation
Pyloric Antrum / cytology,  microbiology*,  physiology
Stomach Diseases / microbiology*
Grant Support
ID/Acronym/Agency:
AI050000/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Bacterial Proteins
Comments/Corrections

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