ArticleGut pathogens2015
Survey of small intestinal and systemic immune responses following murine Arcobacter butzleri infection.
Article in Gut pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- The Immunopathogenic Potential of Arcobacter butzleri - Lessons from a Meta-Analysis of Murine Infection Studies.PloS one · 2016Pooled it
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- Exploring Lead-Like Molecules of Traditional Chinese Medicine for Treatment Quest againstBioMed research international · 2024Article
- Antimicrobial Resistance and Pathogenicity ofAntibiotics (Basel, Switzerland) · 2023Article
- The Effects of Silver Nanoparticles Biosynthesized Using Fig and Olive Extracts on Cutaneous leishmaniasis Induced Inflammation in Female Balb/c Mice.Bioscience reports · 2020Article
- Genomic Characterization ofFrontiers in microbiology · 2019Article
- Toll-Like Receptor-4 Dependent Intestinal Gene Expression During Arcobacter Butzleri Infection of Gnotobiotic Il-10 Deficient Mice.European journal of microbiology & immunology · 2016Article
- Intestinal Expression of Genes Encoding Inflammatory Mediators and Gelatinases During Arcobacter Butzleri Infection of Gnotobiotic Il-10 Deficient Mice.European journal of microbiology & immunology · 2016Article
- Toll-Like Receptor-4 Dependent Small Intestinal Immune Responses Following Murine Arcobacter Butzleri Infection.European journal of microbiology & immunology · 2015Article
- Toll-Like Receptor-4 is Essential for Arcobacter Butzleri-Induced Colonic and Systemic Immune Responses in Gnotobiotic IL-10(-/-) Mice.European journal of microbiology & immunology · 2015Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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