Variable phenotypes of enterocolitis in interleukin 10-deficient mice monoassociated with two different commensal bacteria

Kim, Sandra C.; Tonkonogy, Susan L.; Albright, Carol A.; Tsang, Julia Y. S.; Balish, Edward; Braun, J. S.; Huycke, Mark M.; Sartor, R. Balfour

doi:10.1053/j.gastro.2005.02.009

Cited by 387 publications

(394 citation statements)

References 46 publications

(72 reference statements)

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“…These mice remain disease free with no signs of immune activation when maintained in germfree condition (data not shown) (40). To study the relationship between commensal bacteria and NF-B signaling, we dual associated IL-10 Ϫ/Ϫ ;NF-B EGFP mice with E. faecalis/E.…”

Section: Il-10 ϫ/ϫ ;Nf-b Egfp Mice Develop Pancolitis Following 7 Wk mentioning

confidence: 99%

“…Gnotobiotic technology allows for the well-controlled introduction of a select subset of bacteria into a germfree host and a close and timely monitoring of the elicited host responses (39,40). We first validated the NF-B EGFP mice by monitoring EGFP expression following in vivo LPS stimulation.…”

Section: Nf-b Egfp Gene Reporter Mice (Nf-b Egfp ) Allow For Real-timmentioning

confidence: 99%

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Gnotobiotic IL-10−/−;NF-κBEGFP Mice Reveal the Critical Role of TLR/NF-κB Signaling in Commensal Bacteria-Induced Colitis

Karrasch

Kim

Mühlbauer

et al. 2007

The Journal of Immunology

108

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Commensal bacteria and TLR signaling have been associated with the maintenance of intestinal homeostasis in dextran sodium sulfate-induced intestinal injury. The aim of this study was to determine the in vivo role of TLR/NF-κB activation in a model of commensal bacteria-induced T cell-mediated colitis. A NF-κB reporter gene mouse (NF-κBEGFP) (EGFP, enhanced GFP) was crossed to the colitogenic susceptible strain IL-10−/− and derived into germfree conditions using embryo-transfer technology. Germfree IL-10wt/wt;NF-κBEGFP and IL-10−/−;NF-κBEGFP mice (wt, wild type) were dual associated with the nonpathogenic commensal bacteria strains Enterococcus faecalis and Escherichia coli. EGFP was detected using macroimaging, confocal microscopy, and flow cytometry. IL-10−/−;MyD88−/− mice were used to assess E. faecalis/E. coli-induced TLR-dependent signaling and IL-23 gene expression. Dual-associated IL-10−/−;NF-κBEGFP mice developed severe inflammation by 7 wk. Macroscopic analysis showed elevated EGFP expression throughout the colon of bacteria-associated IL-10−/−;NF-κBEGFP mice. Confocal microscopy analysis revealed EGFP-positive enterocytes during the early phase of bacterial colonization (1 wk) in both IL-10wt/wt and IL-10−/− mice, while the signal shifted toward lamina propria T cells, dendritic cells, neutrophils, and macrophages in IL-10−/− mice during colitis (7 wk). The NF-κB inhibitor BAY 11-7085 attenuated E. faecalis/E. coli-induced EGFP expression and development of colitis. Additionally, E. faecalis/E. coli-induced NF-κB signaling and IL-23 gene expression were blocked in bone marrow-derived dendritic cells derived from IL-10−/−;MyD88−/− mice. We conclude that bacteria-induced experimental colitis involves the activation of TLR-induced NF-κB signaling derived mostly from mucosal immune cells. Blocking TLR-induced NF-κB activity may represent an attractive strategy to treat immune-mediated intestinal inflammation.

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Section: Il-10 ϫ/ϫ ;Nf-b Egfp Mice Develop Pancolitis Following 7 Wk mentioning

confidence: 99%

Section: Nf-b Egfp Gene Reporter Mice (Nf-b Egfp ) Allow For Real-timmentioning

confidence: 99%

Gnotobiotic IL-10−/−;NF-κBEGFP Mice Reveal the Critical Role of TLR/NF-κB Signaling in Commensal Bacteria-Induced Colitis

Karrasch

Kim

Mühlbauer

et al. 2007

The Journal of Immunology

108

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“…These data suggest a link between luminal bacteria and intestinal epithelial repair. In spite of the beneficial role of bacteria in the normal function of the intestine, bacteria have been implicated in the pathogenesis of inflammatory bowel diseases (IBD) 5,6 . These disorders are characterized by chronic, relapsing intestinal inflammation in the absence of a specific pathogen.…”

Section: Introductionmentioning

confidence: 99%

Cox-2 Is Regulated by Toll-Like Receptor-4 (TLR4) Signaling: Role in Proliferation and Apoptosis in the Intestine

Fukata¹,

Chen²,

Klepper³

et al. 2006

Gastroenterology

394

347

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“…32 Conversely, a change in composition of the microbiota has been shown to provoke either type-1 diabetes in genetically prone animals 11 or experimental colitis in other murine models. 33 Mechanistically, a dysbiotic relationship may allow microbial translocation from the gut lumen, leading to a sustained immune activation at local mucosal and submucosal sites. Th is overstimulated immune response can lead to the subsequent induction of infl ammatory and autoimmune conditions.…”

Section: Dysbiosis and Its Potential Consequences On Human Healthmentioning

confidence: 99%

Mucosal immunity: aliment and ailments

Raz

2010

Mucosal Immunology

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Variable phenotypes of enterocolitis in interleukin 10-deficient mice monoassociated with two different commensal bacteria

Abstract: Different commensal bacterial species selectively initiate immune-mediated intestinal inflammation with distinctly different kinetics and anatomic distribution in the same host.

Cited by 387 publications

References 46 publications

Gnotobiotic IL-10−/−;NF-κBEGFP Mice Reveal the Critical Role of TLR/NF-κB Signaling in Commensal Bacteria-Induced Colitis

Gnotobiotic IL-10−/−;NF-κBEGFP Mice Reveal the Critical Role of TLR/NF-κB Signaling in Commensal Bacteria-Induced Colitis

Cox-2 Is Regulated by Toll-Like Receptor-4 (TLR4) Signaling: Role in Proliferation and Apoptosis in the Intestine

Mucosal immunity: aliment and ailments

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