Campylobacter jejuni colonization is associated with a dysbiosis in the cecal microbiota of mice in the absence of prominent inflammation

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dc.contributor.authorLone, Abdul G.
dc.contributor.authorSelinger, L. Brent
dc.contributor.authorUwiera, Richard R. E.
dc.contributor.authorXu, Yong
dc.contributor.authorInglis, G. Douglas
dc.date.accessioned2017-01-16T21:32:42Z
dc.date.available2017-01-16T21:32:42Z
dc.date.issued2013
dc.descriptionSherpa Romeo green journal; open accessen_US
dc.description.abstractBackground: Campylobacter jejuni causes enterocolitis in humans, but does not incite disease in asymptomatic carrier animals. To survive in the intestine, C. jejuni must successfully compete with the microbiota and overcome the host immune defense. Campylobacter jejuni colonization success varies considerably amongst individual mice, and we examined the degree to which the intestinal microbiota was affected in mice (i.e. a model carrier animal) colonized by C. jejuni at high relative to low densities. Methods: Mice were inoculated with C. jejuni or buffer, and pathogen shedding and intestinal colonization were measured. Histopathologic scoring and quantification of mRNA expression for α-defensins, toll-like receptors, and cytokine genes were conducted. Mucosa-associated bacterial communities were characterized by two approaches: multiplexed barcoded pyrosequencing and terminal restriction fragment length polymorphism analysis. Results: Two C. jejuni treatments were established based on the degree of cecal and colonic colonization; C. jejuni Group A animals were colonized at high cell densities, and C. jejuni Group B animals were colonized at lower cell densities. Histological examination of cecal and colonic tissues indicated that C. jejuni did not incite visible pathologic changes. Although there was no significant difference among treatments in expression of mRNA for α-defensins, tolllike receptors, or cytokine genes, a trend for increased expression of toll-like receptors and cytokine genes was observed for C. jejuni Group A. The results of the two methods to characterize bacterial communities indicated that the composition of the cecal microbiota of C. jejuni Group A mice differed significantly from C. jejuni Group B and Control mice. This difference was due to a reduction in load, diversity and richness of bacteria associated with the cecal mucosa of C. jejuni Group A mice. Conclusions: High density colonization by C. jejuni is associated with a dysbiosis in the cecal microbiota independent of prominent inflammation.en_US
dc.description.peer-reviewYesen_US
dc.identifier.citationLone, A. G., Selinger, L. B., Uwiera, R. R. E., Xu, Y., & Inglis, G. D. (2013). Campylobacter jejuni colonization is associated with a dysbiosis in the cecal microbiota of mice in the absence of prominent inflammation. PLoS ONE 8(9), e75325. doi:10.1371/journal.pone.0075325en_US
dc.identifier.urihttps://hdl.handle.net/10133/4759
dc.language.isoen_USen_US
dc.publisherPublic Library of Scienceen_US
dc.publisher.departmentDepartment of Biological Sciencesen_US
dc.publisher.facultyArts and Scienceen_US
dc.publisher.institutionLethbridge Research Centreen_US
dc.publisher.institutionUniversity of Lethbridgeen_US
dc.publisher.institutionUniversity of Albertaen_US
dc.subjectCampylobacter jejunien_US
dc.subjectDysbiosisen_US
dc.subjectCecal microbiotaen_US
dc.subjectMiceen_US
dc.subjectColonizationen_US
dc.subjectMiceen_US
dc.titleCampylobacter jejuni colonization is associated with a dysbiosis in the cecal microbiota of mice in the absence of prominent inflammationen_US
dc.typeArticleen_US
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