Colonization and Inflammation Deficiencies in Mongolian Gerbils Infected by<i>Helicobacter pylori</i>Chemotaxis Mutants

McGee, David J.; Langford, Melanie L.; Watson, Emily L; Carter, J. Elliot; Chen, Yuting; Ottemann, Karen M.

doi:10.1128/iai.73.3.1820-1827.2005

Cited by 93 publications

(134 citation statements)

References 43 publications

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“…Multiple studies of Tlp proteins from the closely related organism H. pylori have demonstrated the functions of these proteins to be complex and not readily apparent when analyzed under in vitro conditions. Thus, several H. pylori tlp mutants have shown contradictory or host-dependent results in terms of colonization potential (3,12,32,39,49). However, the general picture from H. pylori, as well as C. jejuni, is that the Tlp proteins contribute to the physiological fitness of these organisms when facing the challenges encountered during host colonization.…”

Section: Resultsmentioning

confidence: 99%

Energy Taxis Drives Campylobacter jejuni toward the Most Favorable Conditions for Growth

Vegge

Brøndsted

et al. 2009

Appl Environ Microbiol

121

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Campylobacter jejuni is a serious food-borne bacterial pathogen in the developed world. Poultry is a major reservoir, and C. jejuni appears highly adapted to the gastrointestinal tract of birds. Several factors are important for chicken colonization and virulence, including a taxis mechanism for environmental navigation. To explore the mechanism of chemotaxis in C. jejuni, we constructed mutants with deletions of five putative mcp (methyl-accepting chemotaxis protein) genes (tlp1, tlp2, tlp3, docB, and docC). Surprisingly, the deletions did not affect the chemotactic behavior of the mutants compared to that of the parental strain. However, the tlp1, tlp3, docB, and docC mutant strains displayed a 10-fold decrease in the ability to invade human epithelial and chicken embryo cells, hence demonstrating that the corresponding proteins affect the host interaction. LAsparagine, formate, D-lactate, and chicken mucus were identified as new attractants of C. jejuni, and we observed that chemical substances promoting tactic attraction are all known to support the growth of this organism. The attractants could be categorized as carbon sources and electron donors and acceptors, and we furthermore observed a correlation between an attractant's potency and its efficiency as an energy source. The tactic attraction was inhibited by the respiratory inhibitors HQNO (2-n-heptyl-4-hydroxyquinoline N-oxide) and sodium azide, which significantly reduce energy production by oxidative phosphorylation. These findings strongly indicate that energy taxis is the primary force in environmental navigation by C. jejuni and that this mechanism drives the organism toward the optimal chemical conditions for energy generation and colonization.

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Section: Resultsmentioning

confidence: 99%

Energy Taxis Drives Campylobacter jejuni toward the Most Favorable Conditions for Growth

Vegge

Brøndsted

et al. 2009

Appl Environ Microbiol

121

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“…We thus sought a different type of analysis to help characterize the chemotactic response to zinc and nickel. The Brucella broth soft agar migration assay has worked well for H. pylori (Beier et al, 1997;McGee et al, 2005), and so we embarked on adapting this assay to monitor specific chemoeffectors. In the standard version of this assay, bacteria migrate outwards from an inoculation point in response to gradients created either by consuming nutrients or producing waste products.…”

Section: H Pylori Temporal Swimming Assays Work Optimally With Fbs Amentioning

confidence: 99%

A supplemented soft agar chemotaxis assay demonstrates the Helicobacter pylori chemotactic response to zinc and nickel

2013

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Department of Microbiology and Environmental Toxicology at the University of California at Santa Cruz, Santa Cruz, CA, USA Directed motility, or chemotaxis, is required for Helicobacter pylori to establish infection in the stomach, although the full repertoire of this bacterium's chemotactic responses is not yet known. Here we report that H. pylori responds to zinc as an attractant and nickel as a repellent. To reach this conclusion, we employed both a temporal chemotaxis assay based on bacterial reversals and a supplemented soft agar spatial assay. We refined the temporal assay using a previously described chemorepellent, acid, and found that H. pylori requires rich media with serum to maintain optimal swimming motility. Surprisingly, we found that some strains respond to acid as an attractant, and that the TlpC chemoreceptor correlated with whether acid was sensed as an attractant or repellent. Using this same assay, we detected weak repellent responses to nickel and copper, and a varied response to zinc. We thus developed an alternative spatial chemotactic assay called the supplemented soft agar assay, which utilizes soft agar medium supplemented with the test compound. With Escherichia coli, the attractant serine slowed overall bacterial migration, while the repellent nickel increased the speed of overall migration. In H. pylori we detected slowed migration with doubled tryptone media, as well as zinc, consistent with an attractant response. In contrast, nickel increased migration, consistent with repulsion.

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“…Che − mutants have early mouse colonization defects but achieve normal bacterial levels by 1 mo after inoculation (5,16). All cheY mutant-associated phenotypes can be complemented, indicating that loss of cheY is responsible for the chemotaxis and animalcolonization deficits (5,15). Using standard inflammation grading that captures the number and distribution of lymphocytes, we found that inflammation was significantly lower in mice infected for 2 mo with Che − H. pylori than in mice infected with wild-type H. pylori but was greater than in the no-H. pylori control (Fig.…”

Section: Resultsmentioning

confidence: 98%

“…For these experiments, we orally infected mice with either wild-type H. pylori or an isogenic Che − mutant lacking a central chemotaxis protein, CheY. H. pylori cheY mutants have been characterized extensively and found to retain flagella and motility but to lack chemotaxis completely (5,15). Che − mutants have early mouse colonization defects but achieve normal bacterial levels by 1 mo after inoculation (5,16).…”

Section: Resultsmentioning

confidence: 99%

Bacterial chemotaxis modulates host cell apoptosis to establish a T-helper cell, type 17 (Th17)-dominant immune response in Helicobacter pylori infection

Rolig¹,

Carter

Ottemann

2011

Proc. Natl. Acad. Sci. U.S.A.

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The host inflammatory response to chronic bacterial infections often dictates the disease outcome. In the case of the gastric pathogen Helicobacter pylori, host inflammatory responses result in outcomes that range from moderate and asymptomatic to more severe with concomitant ulcer or cancers. It was found recently that H. pylori chemotaxis mutants (Che − ), which lack directed motility but colonize to nearly wild-type levels, trigger less host inflammation. We used these mutants to observe host immune responses that resulted in reduced disease states. Here we report that these mutants are defective for early gastric recruitment of CD4 + T cells compared with wild-type infection. Furthermore, Che − mutant infections lack the Thelper cell, type 17 (Th17) component of the immune response, as measured by cytokine mRNA levels in gastric tissue via intracellular cytokine staining and immunofluorescence. We additionally find that a Che − mutant infection results in significantly less host cell apoptosis than does wild-type infection, in accordance with previous observations that T-helper cell, type 17 responses in Citrobacter rodentium infections are driven by concomitant bacterial and apoptotic cell signals. We propose that bacterial chemotaxis allows H. pylori to access a particular host niche that allows the bacteria to express or deliver proapoptotic host cell factors. This report indicates that chemotaxis plays a role in enhancing apoptosis, suggesting bacterial chemotaxis systems might serve as therapeutic targets for infections whose symptoms arise from host cell apoptosis and tissue damage.T regulatory cells | adaptive immunity | pathogenesis

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Colonization and Inflammation Deficiencies in Mongolian Gerbils Infected byHelicobacter pyloriChemotaxis Mutants

Cited by 93 publications

References 43 publications

Energy Taxis Drives Campylobacter jejuni toward the Most Favorable Conditions for Growth

Energy Taxis Drives Campylobacter jejuni toward the Most Favorable Conditions for Growth

A supplemented soft agar chemotaxis assay demonstrates the Helicobacter pylori chemotactic response to zinc and nickel

Bacterial chemotaxis modulates host cell apoptosis to establish a T-helper cell, type 17 (Th17)-dominant immune response in Helicobacter pylori infection

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