ArticleEuropean journal of microbiology & immunology2015
Toll-Like Receptor-4 Dependent Small Intestinal Immune Responses Following Murine Arcobacter Butzleri Infection.
Article in European journal of microbiology & immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- The Immunopathogenic Potential of Arcobacter butzleri - Lessons from a Meta-Analysis of Murine Infection Studies.PloS one · 2016Pooled it
- Protective Application of Chinese Herbal Compounds and Formulae in Intestinal Inflammation in Humans and Animals.Molecules (Basel, Switzerland) · 2023Review
- Immune Responses to Broad-Spectrum Antibiotic Treatment and Fecal Microbiota Transplantation in Mice.Frontiers in immunology · 2017Article
- 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 Intestinal Gene Expression During Arcobacter Butzleri Infection of Gnotobiotic Il-10 Deficient Mice.European journal of microbiology & immunology · 2016Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sporadic cases of gastroenteritis have been attributed to Arcobacter butzleri infection, but information about the underlying immunopathological mechanisms is scarce. We have recently shown that experimental A. butzleri infection induces intestinal, extraintestinal and systemic immune responses in gnotobiotic IL-10(-/-) mice. The aim of the present study was to investigate the immunopathological role of Toll-like Receptor-4, the receptor for lipopolysaccharide and lipooligosaccharide of Gram-negative bacteria, during murine A. butzleri infection. To address this, gnotobiotic IL-10(-/-) mice lacking TLR-4 were generated by broad-spectrum antibiotic treatment and perorally infected with two different A. butzleri strains isolated from a patient (CCUG 30485) or fresh chicken meat (C1), respectively. Bacteria of either strain stably colonized the ilea of mice irrespective of their genotype at days 6 and 16 postinfection. As compared to IL-10(-/-) control animals, TLR-4(-/-) IL-10(-/-) mice were protected from A. butzleri-induced ileal apoptosis, from ileal influx of adaptive immune cells including T lymphocytes, regulatory T-cells and B lymphocytes, and from increased ileal IFN-γ secretion. Given that TLR-4-signaling is essential for A. butzleri-induced intestinal inflammation, we conclude that bacterial lipooligosaccharide or lipopolysaccharide compounds aggravate intestinal inflammation and may thus represent major virulence factors of Arcobacter. Future studies need to further unravel the molecular mechanisms of TLR-4-mediated A. butzleri-host interactions.
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