Dextran sodium sulphate‐induced colitis activity varies with mouse strain but develops in lipopolysaccharide‐unresponsive mice

Stevceva, Liljana; Pavli, Paul; Buffinton, Gary D.; Wozniak, Andrzej; Doe, William F.

doi:10.1046/j.1440-1746.1999.01806.x

Cited by 42 publications

(40 citation statements)

References 32 publications

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“…Studies in animal models are somewhat more consistent; however, they are not without controversy. Although CH3/HeJ and CH3/HeJBir, TLR4 mutant mice, TLR4 Ϫ/Ϫ , and MyD88 Ϫ/Ϫ mice all exhibit increased susceptibility to DSS-induced colitis (21)(22)(23), synthetic TLR4 antagonists reduce inflammation and disease score in the same model and in the colitis of MDR1a-deficient mice (25). It is yet to be determined whether different spatial and cell type-specific expression patterns of TLR or the different developmental stages of innate and adaptive immunity are responsible for the dichotomy of the roles these molecules might play in neonatal NEC and adult inflammatory bowel disease.…”

Section: Discussionmentioning

confidence: 99%

“…These observations suggest that TLRs participate in the pathogenesis in adult inflammatory bowel disease, but their exact roles are not well understood. In the DSS model of colitis, TLR4 knockout mice exhibit increased susceptibility to colitis (21)(22)(23), but in mice where the myeloid cell-specific deletion of Stat3 results in spontaneous colitis, the introduction of TLR4 Ϫ/Ϫ genotype protected the animals from colitis (24) and a synthetic TLR4 antagonist reduced inflammation and tissue injury in the DSS model of colitis and in colitis of MDR1a-deficient mice (25). Additionally, although multiple studies analyzing genetic polymorphism drew a correlation between UC and CD incidence and/or severity and certain alleles of TLR4, CD14, and NOD2/ CARD15 (26 -36), there are considerable discrepancies among these studies regarding the precise association of various alleles with disease phenotype.…”

Section: N Ecrotizing Enterocolitis (Nec)mentioning

confidence: 99%

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The Roles of Bacteria and TLR4 in Rat and Murine Models of Necrotizing Enterocolitis

Jilling

Simon

Lü

et al. 2006

The Journal of Immunology

342

330

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Bacteria are thought to contribute to the pathogenesis of necrotizing enterocolitis (NEC), but it is unknown whether their interaction with the epithelium can participate in the initiation of mucosal injury or they can act only following translocation across a damaged intestinal barrier. Our aims were to determine whether bacteria and intestinal epithelial TLR4 play roles in a well-established neonatal rat model and a novel neonatal murine model of NEC. Neonatal rats, C57BL/6J, C3HeB/FeJ (TLR4 wild type), and C3H/HeJ (TLR4 mutant) mice were delivered by Cesarean section and were subjected to formula feeding and cold asphyxia stress or were delivered naturally and were mother-fed. NEC incidence was evaluated by histological scoring, and gene expression was quantified using quantitative real-time PCR from cDNA generated from intestinal total RNA or from RNA obtained by laser capture microdissection. Spontaneous feeding catheter colonization or supplementation of cultured bacterial isolates to formula increased the incidence of experimental NEC. During the first 72 h of life, i.e., the time frame of NEC development in this model, intestinal TLR4 mRNA gradually decreases in mother-fed but increases in formula feeding and cold asphyxia stress, correlating with induced inducible NO synthase. TLR4, inducible NO synthase, and inflammatory cytokine induction occurred in the intestinal epithelium but not in the submucosa. NEC incidence was diminished in C3H/HeJ mice, compared with C3HeB/FeJ mice. In summary, bacteria and TLR4 play significant roles in experimental NEC, likely via an interaction of intraluminal bacteria and aberrantly overexpressed TLR4 in enterocytes.

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Section: Discussionmentioning

confidence: 99%

Section: N Ecrotizing Enterocolitis (Nec)mentioning

confidence: 99%

The Roles of Bacteria and TLR4 in Rat and Murine Models of Necrotizing Enterocolitis

Jilling

Simon

Lü

et al. 2006

The Journal of Immunology

342

330

View full text Add to dashboard Cite

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“…Biopsy samples (B10 mg) prepared from colon tissue were snap frozen in liquid nitrogen. The intestine was fixed in 4% paraformaldehyde and prepared for both immunohistochemistry and pathology evaluation using an established method (Stevceva et al, 1999;Williams et al, 2001;Pflegerl et al, 2009). Flushed lumen contents were homogenized, collected by centrifugation and either snap frozen for DNA and RNA purification or fixed in 2% paraformaldehyde overnight at 4 1C and then stored in 70% ethanol/30% phosphate-buffered saline at À 20 1C until analysis (see Supplemental Methods for more details).…”

Section: Animal Experimentsmentioning

confidence: 99%

Phylotype-level 16S rRNA analysis reveals new bacterial indicators of health state in acute murine colitis

et al. 2012

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Human inflammatory bowel disease and experimental colitis models in mice are associated with shifts in intestinal microbiota composition, but it is unclear at what taxonomic/phylogenetic level such microbiota dynamics can be indicative for health or disease. Here, we report that dextran sodium sulfate (DSS)-induced colitis is accompanied by major shifts in the composition and function of the intestinal microbiota of STAT1 À / À and wild-type mice, as determined by 454 pyrosequencing of bacterial 16S rRNA (gene) amplicons, metatranscriptomics and quantitative fluorescence in situ hybridization of selected phylotypes. The bacterial families Ruminococcaceae, Bacteroidaceae, Enterobacteriaceae, Deferribacteraceae and Verrucomicrobiaceae increased in relative abundance in DSS-treated mice. Comparative 16S rRNA sequence analysis at maximum possible phylogenetic resolution identified several indicator phylotypes for DSS treatment, including the putative mucin degraders Akkermansia and Mucispirillum. The analysis additionally revealed strongly contrasting abundance changes among phylotypes of the same family, particularly within the Lachnospiraceae. These extensive phylotype-level dynamics were hidden when reads were grouped at higher taxonomic levels. Metatranscriptomic analysis provided insights into functional shifts in the murine intestinal microbiota, with increased transcription of genes associated with regulation and cell signaling, carbohydrate metabolism and respiration and decreased transcription of flagellin genes during inflammation. These findings (i) establish the first in-depth inventory of the mouse gut microbiota and its metatranscriptome in the DSS colitis model, (ii) reveal that family-level microbial community analyses are insufficient to reveal important colitisassociated microbiota shifts and (iii) support a scenario of shifting intra-family structure and function in the phylotype-rich and phylogenetically diverse Lachnospiraceae in DSS-treated mice.

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“…16 The clinical signs were analysed separately and correlated with the histological score. The final formula for the DAI was evaluated by correlation with the histological score.…”

Section: Disease Activity Indexmentioning

confidence: 99%

Eosinophilia is attenuated in experimental colitis induced in IL-5 deficient mice

Stevceva

Pavli²,

Husband

et al. 2000

Genes Immun

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Tissue eosinophilia is a feature of idiopathic inflammatory bowel disease and other forms of colonic inflammation but it is not clear whether the role of eosinophils in the disease process is to contribute to tissue damage. Interleukin 5 (IL-5) stimulates production and activation of eosinophils in vitro and enhances immunoglobulin A (IgA) production. As very little is known about the function of IL-5 in the colon, the aim of this study was to assess its role in colonic inflammation. IL-5 deficient mice were studied using the dextran sulphate sodium (DSS)-induced colitis model and the results compared to a congenic IL-5+/+ strain. The absence of IL-5 resulted in reduction of tissue eosinophilia (P Ͻ 0.0001) but was not reflected in differences in the severity of the disease (P Ͼ 0.5) or in the extent of tissue damage in this model of colitis. Numbers of immunoglobulin-containing cells in IL-5 deficient mice were similar to those in the IL-5+ mice. We conclude that the main role of IL-5 in DSS-induced colonic inflammation is to attract a population of eosinophils which do not appear to contribute significantly to the initiation or development of tissue damage in this model of colitis. Genes and Immunity (2000) 1, 213-218.

show abstract

Dextran sodium sulphate‐induced colitis activity varies with mouse strain but develops in lipopolysaccharide‐unresponsive mice

Cited by 42 publications

References 32 publications

The Roles of Bacteria and TLR4 in Rat and Murine Models of Necrotizing Enterocolitis

The Roles of Bacteria and TLR4 in Rat and Murine Models of Necrotizing Enterocolitis

Phylotype-level 16S rRNA analysis reveals new bacterial indicators of health state in acute murine colitis

Eosinophilia is attenuated in experimental colitis induced in IL-5 deficient mice

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