Enhancing adherence of Arcobacter butzleri after serial intraperitoneal passages in mice

Fernández, Heriberto; Flores, Sandra; Villanueva, María Paz; Medina, Gustavo; Carrizo, Macarena

doi:10.1016/s0325-7541(13)70002-6

Cited by 7 publications

(6 citation statements)

References 15 publications

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“…butzleri infected gnotobiotic IL-10 -/- mice [ 13 – 16 ], only one single in vivo study in mice had been published showing that the adherent properties of initially low-adherent A . butzleri strains were enhanced upon serial intraperitoneal passages [ 33 ]. Our murine A .…”

Section: Discussionmentioning

confidence: 99%

The Immunopathogenic Potential of Arcobacter butzleri – Lessons from a Meta-Analysis of Murine Infection Studies

et al. 2016

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BackgroundOnly limited information is available about the immunopathogenic properties of Arcobacter infection in vivo. Therefore, we performed a meta-analysis of published data in murine infection models to compare the pathogenic potential of Arcobacter butzleri with Campylobacter jejuni and commensal Escherichia coli as pathogenic and harmless reference bacteria, respectively.Methodology / Principal FindingsGnotobiotic IL-10-/- mice generated by broad-spectrum antibiotic compounds were perorally infected with A. butzleri (strains CCUG 30485 or C1), C. jejuni (strain 81-176) or a commensal intestinal E. coli strain. Either strain stably colonized the murine intestines upon infection. At day 6 postinfection (p.i.), C. jejuni infected mice only displayed severe clinical sequelae such as wasting bloody diarrhea. Gross disease was accompanied by increased numbers of colonic apoptotic cells and distinct immune cell populations including macrophages and monocytes, T and B cells as well as regulatory T cells upon pathogenic infection. Whereas A. butzleri and E. coli infected mice were clinically unaffected, respective colonic immune cell numbers increased in the former, but not in the latter, and more distinctly upon A. butzleri strain CCUG 30485 as compared to C1 strain infection. Both, A. butzleri and C. jejuni induced increased secretion of pro-inflammatory cytokines such as IFN-γ, TNF, IL-6 and MCP-1 in large, but also small intestines. Remarkably, even though viable bacteria did not translocate from the intestines to extra-intestinal compartments, systemic immune responses were induced in C. jejuni, but also A. butzleri infected mice as indicated by increased respective pro-inflammatory cytokine concentrations in serum samples at day 6 p.i.Conclusion / SignificanceA. butzleri induce less distinct pro-inflammatory sequelae as compared to C. jejuni, but more pronounced local and systemic immune responses than commensal E. coli in a strain-dependent manner. Hence, data point towards that A. butzleri is more than a commensal in vertebrate hosts.

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Section: Discussionmentioning

confidence: 99%

The Immunopathogenic Potential of Arcobacter butzleri – Lessons from a Meta-Analysis of Murine Infection Studies

et al. 2016

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“…Results from the few studies to date, however, are rather conflicting and highly dependent on the animal species, the breed and/or on the respective A. butzleri strain under investigation [ 1 ]. To our knowledge, only one single Arcobacter infection study has been performed in mice so far demonstrating that following serial intraperitoneal passages in mice, the adherent capabilities of initially low-adherent A. butzleri strains were enhanced [ 39 ]. Previously, our group has established several murine C. jejuni infection models (reviewed in [ 40 ]).…”

Section: Discussionmentioning

confidence: 99%

Survey of small intestinal and systemic immune responses following murine Arcobacter butzleri infection

et al. 2015

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BackgroundArcobacter (A.) butzleri has been described as causative agent for sporadic cases of human gastroenteritis with abdominal pain and acute or prolonged watery diarrhea. In vitro studies revealed distinct adhesive, invasive and cytotoxic properties of A. butzleri. Information about the underlying immunopathological mechanisms of infection in vivo, however, are scarce. The aim of this study was to investigate the immunopathological properties of two different A.butzleri strains in a well-established murine infection model.ResultsGnotobiotic IL-10−/− mice, in which the intestinal microbiota was depleted by broad-spectrum antibiotic treatment, were perorally infected with two different A. butzleri strains isolated from a diseased patient (CCUG 30485) or fresh chicken meat (C1), respectively. Eventhough bacteria of either strain could stably colonize the intestinal tract at day 6 and day 16 postinfection (p.i.), mice did not exert infection induced symptoms such as diarrhea or wasting. In small intestines of infected mice, however, increased numbers of apoptotic cells could be detected at day 16, but not day 6 following infection with either strain. A strain-dependent influx of distinct immune cell populations such as T and B cells as well as of regulatory T cells could be observed upon A. butzleri infection which was accompanied by increased small intestinal concentrations of pro-inflammatory cytokines such as TNF, IFN-γ, MCP-1 and IL-6. Remarkably, inflammatory responses following A. butzleri infection were not restricted to the intestinal tract, given that the CCUG 30485 strain induced systemic immune responses as indicated by increased IFN-γ concentrations in spleens at day 6, but not day 16 following infection.ConclusionUpon peroral infection A. butzleri stably colonized the intestinal tract of gnotobiotic IL-10−/− mice. The dynamics of distinct local and systemic inflammatory responses could be observed in a strain-dependent fashion pointing towards an immunopathogenic potential of A. butzleri in vivo. These results indicate that gnotobiotic IL-10−/− mice are well suited to further investigate the molecular mechanisms underlying arcobacteriosis in vivo.

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“…Similar results from an evaluation of the virulence potential of Shiga toxin (Stx)-producing Escherichia coli (STEC) were also observed when mice were infected with a lower dose of the recovered bacteria that had been recovered after serial passage in a murine model (Fernandez-Brando et al, 2012). Other studies have also shown that the serial passage process through in vitro or in vivo models leads to changes in the virulence potential of pathogens, including Helicobacter pylori, Escherichia coli, Xenorhabdus nematophila, Arcobacter butzleri, Salmonella enterica , and Shigella flexneri (Fernández et al, 2000, 2013; Bleich et al, 2005; Chapuis et al, 2011; Fernandez-Brando et al, 2012; Liu et al, 2015). Changes in the virulence potential of these pathogens, as well as in 258_ equi , show that this strategy promotes the activation of genes related to bacterial pathogenesis.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, several studies have used mice as a model for studying both the pathogenic process (Jolly, 1965; Zaki, 1966; Nieto et al, 2009) and vaccination testing against infection by C. pseudotuberculosis (Simmons et al, 1997; Lan et al, 1999; Gorman et al, 2010; Ribeiro et al, 2014; Droppa-Almeida et al, 2016). In regards to host-bacteria interactions, some work has explored the serial passage process of bacterial pathogens in vitro or in an in vivo model to identify factors that might be involved in virulence (Fernández et al, 2000, 2013; Bleich et al, 2005; Chapuis et al, 2011; Fernandez-Brando et al, 2012; Liu et al, 2015). In this study, we adopted an in vivo assay in which the strain 258_ equi was experimentally inoculated in mice followed by high-throughput proteomic analysis.…”

Section: Introductionmentioning

confidence: 99%

Quantitative Proteomic Analysis Reveals Changes in the Benchmark Corynebacterium pseudotuberculosis Biovar Equi Exoproteome after Passage in a Murine Host

Silva

Carvalho

Dorella

et al. 2017

Front. Cell. Infect. Microbiol.

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Corynebacterium pseudotuberculosis biovar equi is the etiologic agent of ulcerative lymphangitis. To investigate proteins that could be related to the virulence of this pathogen, we combined an experimental passage process using a murine model and high-throughput proteomics with a mass spectrometry, data-independent acquisition (LC-MSE) approach to identify and quantify the proteins released into the supernatants of strain 258_equi. To our knowledge, this approach allowed characterization of the exoproteome of a C. pseudotuberculosis equi strain for the first time. Interestingly, the recovery of this strain from infected mouse spleens induced a change in its virulence potential, and it became more virulent in a second infection challenge. Proteomic screening performed from culture supernatant of the control and recovered conditions revealed 104 proteins that were differentially expressed between the two conditions. In this context, proteomic analysis of the recovered condition detected the induction of proteins involved in bacterial pathogenesis, mainly related to iron uptake. In addition, KEGG enrichment analysis showed that ABC transporters, bacterial secretion systems and protein export pathways were significantly altered in the recovered condition. These findings show that secretion and secreted proteins are key elements in the virulence and adaptation of C. pseudotuberculosis. Collectively, bacterial pathogenesis-related proteins were identified that contribute to the processes of adherence, intracellular growth and evasion of the immune system. Moreover, this study enhances our understanding of the factors that may influence the pathogenesis of C. pseudotuberculosis.

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Enhancing adherence of Arcobacter butzleri after serial intraperitoneal passages in mice

Cited by 7 publications

References 15 publications

The Immunopathogenic Potential of Arcobacter butzleri – Lessons from a Meta-Analysis of Murine Infection Studies

The Immunopathogenic Potential of Arcobacter butzleri – Lessons from a Meta-Analysis of Murine Infection Studies

Survey of small intestinal and systemic immune responses following murine Arcobacter butzleri infection

Quantitative Proteomic Analysis Reveals Changes in the Benchmark Corynebacterium pseudotuberculosis Biovar Equi Exoproteome after Passage in a Murine Host

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