ArticleEuropean journal of microbiology & immunology2015
Toll-Like Receptor-4 is Essential for Arcobacter Butzleri-Induced Colonic and Systemic Immune Responses in Gnotobiotic IL-10(-/-) Mice.
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, 8 citations in OpenAlex.
- The Immunopathogenic Potential of Arcobacter butzleri - Lessons from a Meta-Analysis of Murine Infection Studies.PloS one · 2016Pooled it
- Pathogenicity of Arcobacter cryaerophilus in two human intestinal cell lines.Gut pathogens · 2025Article
- Dexmedetomidine attenuates lipopolysaccharide-induced acute liver injury in rats by inhibiting caveolin-1 downstream signaling pathway.Bioscience reports · 2021Article
- 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
Corrections and comments
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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
Arcobacter butzleri causes sporadic cases of gastroenteritis, but the underlying immunopathological mechanisms of infection are unknown. We have recently demonstrated that A. butzleri-infected gnotobiotic IL-10(-/-) mice were clinically unaffected but exhibited intestinal and systemic inflammatory immune responses. For the first time, we here investigated the role of Toll-like receptor (TLR)-4, the main receptor for lipopolysaccharide and lipooligosaccharide of Gram-negative bacteria, in murine arcobacteriosis. Gnotobiotic TLR-4/IL-10-double deficient (TLR-4(-/-) IL-10(-/-)) and IL-10(-/-) control mice generated by broad-spectrum antibiotics were perorally infected with A. butzleri. Until day 16 postinfection, mice of either genotype were stably colonized with the pathogen, but fecal bacterial loads were approximately 0.5-2.0 log lower in TLR-4(-/-) IL-10(-/-) as compared to IL-10(-/-) mice. A. butzleri-infected TLR-4(-/-) IL-10(-/-) mice displayed less pronounced colonic apoptosis accompanied by lower numbers of macrophages and monocytes, T lymphocytes, regulatory T-cells, and B lymphocytes within the colonic mucosa and lamina propria as compared to IL-10(-/-) mice. Furthermore, colonic concentrations of nitric oxide, TNF, IL-6, MCP-1, and, remarkably, IFN-γ and IL-12p70 serum levels were lower in A. butzleri-infected TLR-4(-/-) IL-10(-/-) versus IL-10(-/-) mice. In conclusion, TLR-4 is involved in mediating murine A. butzleri infection. Further studies are needed to investigate the molecular mechanisms underlying Arcobacter-host interactions in more detail.
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