Arcobacter butzleri induces a pro-inflammatory response in THP-1 derived macrophages and has limited ability for intracellular survival

Bruegge, Jennifer zur; Hanisch, Carlos; Einspanier, Ralf; Alter, Thomas; Gölz, Greta; Sharbati, Soroush

doi:10.1016/j.ijmm.2014.08.017

Cited by 15 publications

(12 citation statements)

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“…butzleri infection of THP-derived macrophages resulted in an increased activity of caspase-3 among caspase-7 and -8 which was accompanied by an upregulated expression of pro-inflammatory cytokines such as TNF, IL-6 and IL-12 [ 25 ] as shown in colon and serum of infected mice in our present in vivo study. Interestingly, despite initially increased caspase-3 levels, DNA damage was virtually absent suggesting potential counter-regulatory measures on the cellular level in THP-1 cells [ 25 ]. In line with this, we here demonstrate that A .…”

Section: Discussionmentioning

confidence: 69%

Arcobacter butzleri Induce Colonic, Extra-Intestinal and Systemic Inflammatory Responses in Gnotobiotic IL-10 Deficient Mice in a Strain-Dependent Manner

et al. 2015

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BackgroundThe immunopathological impact of human Arcobacter (A.) infections is under current debate. Episodes of gastroenteritis with abdominal pain and acute or prolonged watery diarrhea were reported for A. butzleri infected patients. Whereas adhesive, invasive and cytotoxic capacities have been described for A. butzleri in vitro, only limited information is available about the immunopathogenic potential and mechanisms of infection in vivo.Methodology/Principal FindingsGnotobiotic IL-10-/- mice were generated by broad-spectrum antibiotic treatment and perorally infected with the A. butzleri strains CCUG 30485 and C1 shown to be invasive in cell culture assays. Bacterial colonization capacities, clinical conditions, intestinal, extra-intestinal and systemic immune responses were monitored at day six and 16 postinfection (p.i.). Despite stable intestinal A. butzleri colonization at high loads, gnotobiotic IL-10-/- mice were virtually unaffected and did not display any overt symptoms at either time point. Notably, A. butzleri infection induced apoptosis of colonic epithelial cells which was paralleled by increased abundance of proliferating cells. Furthermore A. butzleri infection caused a significant increase of distinct immune cell populations such as T and B cells, regulatory T cells, macrophages and monocytes in the colon which was accompanied by elevated colonic TNF, IFN-γ, nitric oxide (NO), IL-6, IL-12p70 and MCP-1 concentrations. Strikingly, A. butzleri induced extra-intestinal and systemic immune responses as indicated by higher NO concentrations in kidney and increased TNF, IFN-γ, IL-12p70 and IL-6 levels in serum samples of infected as compared to naive mice. Overall, inflammatory responses could be observed earlier in the course of infection by the CCUG 30485 as compared to the C1 strain.Conclusion/SignificancePeroral A. butzleri infection induced not only intestinal but also extra-intestinal and systemic immune responses in gnotobiotic IL-10-/- mice in a strain-dependent manner. These findings point towards an immunopathogenic potential of A. butzleri in vertebrate hosts.

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Section: Discussionmentioning

confidence: 69%

Arcobacter butzleri Induce Colonic, Extra-Intestinal and Systemic Inflammatory Responses in Gnotobiotic IL-10 Deficient Mice in a Strain-Dependent Manner

et al. 2015

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“…It has also been reported that Arcobacter spp. induced IL‐8 expression in human Caco‐2 and porcine IPI‐2I cell lines (Ho et al, ), and that IL‐8 and TNF‐α were highly induced in THP‐1‐derived macrophages infected by Arcobacter butzleri (Bruegge et al, ). The disruption and dysbiosis of microbiota homeostasis in group ASTX500 might, at least partly, explain the profound intestinal inflammation in this group.…”

Section: Discussionmentioning

confidence: 99%

The effects of dietary astaxanthin on intestinal health of juvenile tiger puffer Takifugu rubripes in terms of antioxidative status, inflammatory response and microbiota

Liao

et al. 2018

Aquacult Nutr

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A 74‐day feeding trial was conducted to evaluate the effects of dietary astaxanthin (ASTX) on antioxidative status, inflammatory response and microbiota in the intestine of tiger puffer. Four diets differed only in ASTX content, that is, 0 (Control), 50 (ASTX50), 100 (ASTX100) and 500 (ASTX500) mg/kg. Compared with Control, ASTX50 and ASTX100 significantly reduced the malondialdehyde content and spared the activities of antioxidative enzymes in hindgut; however, ASTX500 had higher activity and gene expression of antioxidative enzymes. Nuclear factor‐erythroid 2 p45‐related factor 2 (Nrf2) and Kelch‐like ECH‐associated protein 1 (Keap1) signalling were probably involved in the transcriptional regulation of antioxidative enzymes by dietary ASTX. Compared with Control and ASTX500, ASTX50 and ASTX100 decreased the leucocyte infiltration in the lamina propria of hindgut and down‐regulated the gene expression of tumour necrosis factor‐α (TNF‐α) and interleukin‐8 (IL‐8). ASTX markedly affected the overall structure of intestinal microbiota. The relative abundance of Arcobacter, which has harmful properties, was the lowest in ASTX100 but the highest in ASTX500. In conclusion, dietary ASTX at 50 or 100 mg/kg improved the antioxidative status, alleviated the inflammation and favourably modulated the microbiota in tiger puffer intestine, but excess ASTX exerted contrary effects.

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“…This is further underlining that the murine gnotobiotic IL-10 −/− applied here is well suited to unravel pathogen-host-interactions. Despite subsequent activation of caspase-3, -7 and -8, macrophages survived A. butzleri infection without any signs of DNA damage pointing towards cellular counter-regulatory measures [ 42 ]. Given that in our study higher ileal apoptotic as well as Ki67+ proliferating cell numbers could be observed at day 16 as compared to day 6 following C1 strain infection, absence of macroscopic disease might have also been due to distinct counter-regulatory measures despite stable bacterial colonization.…”

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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Arcobacter butzleri induces a pro-inflammatory response in THP-1 derived macrophages and has limited ability for intracellular survival

Cited by 15 publications

References 43 publications

Arcobacter butzleri Induce Colonic, Extra-Intestinal and Systemic Inflammatory Responses in Gnotobiotic IL-10 Deficient Mice in a Strain-Dependent Manner

Arcobacter butzleri Induce Colonic, Extra-Intestinal and Systemic Inflammatory Responses in Gnotobiotic IL-10 Deficient Mice in a Strain-Dependent Manner

The effects of dietary astaxanthin on intestinal health of juvenile tiger puffer Takifugu rubripes in terms of antioxidative status, inflammatory response and microbiota

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

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