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.authorSelinger, L. Brent
dc.contributor.authorInglis, G. Douglas
dc.contributor.authorUwiera, Richard R. E.
dc.contributor.authorLone, Abdul
dc.contributor.authorXu, Yong
dc.date.accessioned2025-05-01T11:56:17Z
dc.date.available2025-05-01T11:56:17Z
dc.date.issued2013
dc.descriptionBackground 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, toll-like 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.
dc.identifier.doihttps://doi.org/10.7939/R3RV0DD71
dc.language.isoen
dc.relationhttp://dx.doi.org/10.1371/journal.pone.0075325
dc.relation.isversionofLone, A., 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 [15 pages]. http://dx.doi.org/10.1371/journal.pone.0075325
dc.rightsAttribution 4.0 International
dc.subjectGastrointestinal Tract
dc.subjectCampylobacter jejuni
dc.subjectMicrobiome
dc.subjectBacteria
dc.subjectCecum
dc.subjectCytokines
dc.subjectToll-Like Receptors
dc.subjectPolymerase Chain Reaction
dc.titleCampylobacter jejuni colonization is associated with a dysbiosis in the cecal microbiota of mice in the absence of prominent inflammation
dc.typehttp://purl.org/coar/resource_type/c_6501 http://purl.org/coar/version/c_970fb48d4fbd8a85
ual.jupiterAccesshttp://terms.library.ualberta.ca/public

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