Oral administration of dextran sodium sulphate induces a caecum‐localized colitis in rabbits

Leonardi, Irina; Nicholls, Flora; Atrott, Kirstin; Cee, Alexandra; Tewes, Bernhard; Greinwald, Roland; Rogler, Gerhard; Frey-Wagner, Isabelle

doi:10.1111/iep.12117

Cited by 12 publications

(3 citation statements)

References 50 publications

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“…Since Kirsner successfully induced colitis model in rabbits for the rst time in 1957, for more than 60 years, researchers have tried to establish different types of animal models with mice, rats, rabbits, monkeys and sheep as research objects to study the pathological mechanism and pharmacodynamic screening of UC [13][14][15][16][17] . C57BL / 6 mice are the main model animals because of their small size, convenient feeding and histopathology more similar to human UC [18] .…”

Section: Introductionmentioning

confidence: 99%

Behavioral abnormalities in C57BL/6 mice with chronic ulcerative colitis induced by DSS

Zhou

Yang

et al. 2022

Preprint

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Background: Clinical epidemiological studies have found that some patients with ulcerative colitis (UC) are prone to mental disorders. DSS-induced acute and chronic UC models are often used to evaluate the efficacy of anti-UC drugs. However, whether DSS has an effect on mouse behavior has not been reported. Methods: Acute and chronic UC models were induced by 3% DSS and 1.5% DSS, respectively. The bloody stool, the changes in the colon length, and histopathological changes in the colon were used to evaluate the success of the animal model. The behavior of mice was evaluated by open field experiment, tail suspension experiment and Sucrose preference test. Results: The weight of mice in 3% DSS group decreased significantly, the DAI score increased significantly, the colon length of mice was significantly shortened, and the structure of colonic crypts was abnormal, which showed inflammatory cell infiltration and shrinkage of crypts. Compared with the control group, the immobility time of 3%DSS group mice in the tail suspension test and forced swimming test had no effect, the number of running and grooming times was significantly reduced, and there was no significant difference in the number of standing times. No abnormality was observed in HE staining of the hippocampus. However, in 1.5% DSS-induced chronic UC model, behavioral and hippocampal abnormalities were observed not only UC symptoms. Conclusions: Acute UC induced by 3% DSS had little effect on mouse behavior, while chronic UC induced by 1.5% DSS had a significant effect on mouse behavior.

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Section: Introductionmentioning

confidence: 99%

Behavioral abnormalities in C57BL/6 mice with chronic ulcerative colitis induced by DSS

Zhou

Yang

et al. 2022

Preprint

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“…However, the therapeutic mechanism remains unclear. In the current study, the therapeutic effects of SIN were investigated in a dextran sulfate sodium (DSS)-induced colitis model, which possesses similar fundamental clinical and histological features to human UC ( 17 ).…”

Section: Introductionmentioning

confidence: 99%

Sinomenine alleviates dextran sulfate sodium‑induced colitis via the Nrf2/NQO‑1 signaling pathway

et al. 2018

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Sinomenine (SIN), a pure alkaloid isolated from Sinomenium acutum, has been widely used in arthritis for its anti-inflammatory effect, but little is known about the effect of SIN on human ulcerative colitis (UC). In the present study, the effect and mechanism of SIN was examined in a dextran sulfate sodium (DSS)-induced murine colitis model, which mimics human UC. Oral administration of SIN significantly suppressed the elevated disease activity index and ameliorated colonic histological damage in a DSS-induced colitis model. Tumor necrosis factor-α, interleukin-6 and inducible nitric oxide synthase levels were also reduced as detected by reverse transcription-quantitative polymerase chain reaction. In addition, SIN reversed the decreased colon length and colonic superoxide dismutase activity. Furthermore, western blot analysis revealed that nuclear factor-erythroid 2-related factor 2 (Nrf2) and its downstream genes, heme oxygenase-1 and NADP(H) quinone oxidoreductase 1 (NQO-1), were markedly activated by SIN. The current results indicated that SIN alleviated DSS-induced colitis in mice, which may be due to its antioxidant properties and was at least in part dependent on the Nrf2/NQO-1 signaling pathway. Therefore, SIN may have potential applications as a protective drug for patients with UC.

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“…Tissues were fixed overnight at 4°C in 4% paraformaldehyde, embedded in paraffin, sectioned, and stained with H&E. Histological analyses of morphological features and inflammation were performed by a board-certified pathologist according to a modified criterion described in a previous publication (16). The scoring system is shown in Supplementary Table 2.…”

Section: Histological Assessmentmentioning

confidence: 99%

Pyruvate: Ferredoxin oxidoreductase is involved in IgA-related microbiota dysbiosis and intestinal inflammation

et al. 2022

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IntroductionInflammatory bowel diseases (IBDs) are associated with both immune abnormalities and dysbiosis, characterized by a loss of Faecalibacterium prausnitzii (F. prausnitzii). However, the reason for F. prausnitzii deficiency remains unclear.Methods16S rDNA sequencing and IgA enzyme-linked immunosorbent assay (ELISA) were applied to identify bacterial community and IgA changes in ulcerative colitis (UC) patients. Forced immunization with F. prausnitzii in rabbits was conducted. To screen for potential IgA-reactive proteins in F. prausnitzii lysates, we performed western blotting and mass spectrometry analyses. Pyruvate: ferredoxin oxidoreductase (PFOR) was cloned and purified, then the immunoreactivity of PFOR was verified in peripheral blood mononuclear cells (PBMCs) through PCR, ELISpot assay and single-cell sequencing (scRNA-seq). Finally, the UC fecal dysbiosis was re-analyzed in the context of the phylogenetic tree of PFOR.ResultsF. prausnitzii was underrepresented in UC patients with elevated F. prausnitzii-reactive IgA in the fecal supernatant. Forced immunization with F. prausnitzii in rabbits led to high interferon-γ (IFN-γ) transcription in the colon, along with beta diversity disturbance and intestinal inflammation. PFOR was identified as an IgA-binding antigen of F. prausnitzii and the immunoreactivity was validated in PBMCs, which showed elevated expression of inflammatory cytokines. The scRNA-seq revealed enhanced signals in both T regulatory cells (Tregs) and monocytes after PFOR incubation. Furthermore, phylogenetic analysis revealed that PFOR was a common but conserved protein among the gut bacteria.DiscussionOur results collectively suggest that PFOR is a bioactive protein in the immune system and may contribute to host-microbial crosstalk. Conserved but bioactive microbial proteins, such as PFOR, warrant more attention in future host-microbial interaction studies.

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Oral administration of dextran sodium sulphate induces a caecum‐localized colitis in rabbits

Cited by 12 publications

References 50 publications

Behavioral abnormalities in C57BL/6 mice with chronic ulcerative colitis induced by DSS

Behavioral abnormalities in C57BL/6 mice with chronic ulcerative colitis induced by DSS

Sinomenine alleviates dextran sulfate sodium‑induced colitis via the Nrf2/NQO‑1 signaling pathway

Pyruvate: Ferredoxin oxidoreductase is involved in IgA-related microbiota dysbiosis and intestinal inflammation

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