Intravenous Injection of Endogenous Microbial Components Abrogates DSS-Induced Colitis

Sydora, Beate C.; Albert, Eric J.; Foshaug, Rae; Doyle, Jason; Churchill, Thomas A.; Fedorak, Richard N.

doi:10.1007/s10620-011-1878-5

Cited by 9 publications

(6 citation statements)

References 41 publications

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“…It has been recognized that systemic inflammatory response is hallmark of DSS-induced colitis [20], [21]. Thus, we examined the influence of TNF-R1 or 2 knockout on the disease parameters.…”

Section: Resultsmentioning

confidence: 99%

Opposite Role of Tumor Necrosis Factor Receptors in Dextran Sulfate Sodium-Induced Colitis in Mice

Wang

Han²,

et al. 2012

PLoS ONE

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Tumor necrosis factor-α (TNF-α) is a key factor for the pathogenesis of inflammatory bowel diseases (IBD), whose function is known to be mediated by TNF receptor 1 (TNFR1) or 2. However, the precise role of the two receptors in IBD remains poorly understood. Herein, acute colitis was induced by dextran sulfate sodium (DSS) instillation in TNFR1 or 2−/− mice. TNFR1 ablation led to exacerbation of signs of colitis, including more weight loss, increased mortality, colon shortening and oedema, severe intestinal damage, and higher levels of myeloperoxidase compared to wild-type counterparts. While, TNFR2 deficiency had opposite effects. This discrepancy was reflected by alteration of proinflammatory cytokine and chemokine production in the colons. Importantly, TNFR1 ablation rendered enhanced apoptosis of colonic epithelial cells and TNFR2 deficiency conferred pro-apoptotic effects of lamina propria (LP)-immune cells, as shown by the decreased ratio of Bcl-2/Bax and enhanced nuclear factor (NF)-κB activity.

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Section: Resultsmentioning

confidence: 99%

Opposite Role of Tumor Necrosis Factor Receptors in Dextran Sulfate Sodium-Induced Colitis in Mice

Wang

Han²,

et al. 2012

PLoS ONE

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“…26,27 Therefore, we investigated the influence of TNFR1 or TNFR2 deficiency on the disease parameters. Indeed, WT mice displayed visible splenomegaly in terms of spleen weights after DSS.…”

Section: Ablation Of Tnfr1 Augments Systemic Inflammatory Responsesmentioning

confidence: 99%

Protective role of tumor necrosis factor (TNF) receptors in chronic intestinal inflammation: TNFR1 ablation boosts systemic inflammatory response

Wang¹,

Han²,

Chen³

et al. 2013

Laboratory Investigation

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Tumor necrosis factor-a (TNF-a) acts as a key factor for the development of inflammatory bowel diseases (IBDs), whose function is known to be mediated by TNF receptor 1 (TNFR1) or TNFR2. However, the precise role of the two receptors in IBD remains poorly understood. Herein, chronic colitis was established by oral administration of dextran sulfate sodium (DSS) in TNFR1 or TNFR2 À / À mice. Unexpectedly, TNFR1 or TNFR2 deficiency led to exacerbation of signs of colitis compared with wild-type (WT) counterparts. Of note, TNFR1 ablation rendered significantly increased mortality compared with TNFR2 and WT mice after DSS. Aggravated pathology of colitis in TNFR1 À / À or TNFR2 À / À mice correlated with elevated colonic expression of proinflammatory cytokines and chemokines. Importantly, ablation of TNFR1 or TNFR2 increased apoptosis of colonic epithelial cells, which might be due to the heightened ratio of Bax/Bcl-2 and increased expression of caspase-8. Intriguingly, despite comparable intensity of intestinal inflammation in TNFR-deficient mice after DSS, systemic inflammatory response (including splenomegaly and myeloid expansion) was augmented dramatically in TNFR1 À / À mice, instead of TNFR2 À / À mice. Granulocyte macrophage colony-stimulating factor (GMCSF) was identified as a key mediator in this process, as neutralization of GMCSF dampened peripheral inflammatory reaction and reduced mortality in TNFR1 À / À mice. These data suggest that signaling via TNFR1 or TNFR2 has a protective role in chronic intestinal inflammation, and that lacking TNFR1 augments systemic inflammatory response in GMCSF-dependent manner.

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“…In this regard, the antibiotics metronidazole and ciprofloxacin ameliorate acute, although not chronic, DSS colitis in mice, and oral administration of bacterial sonicates dampens DSS colitis, possibly via tolerogenic mechanisms. 9,10 Taking in consideration these facts and the relationship between the intestinal microbiota and the intestinal immune system and barrier function, we formulated the hypothesis that these two elements may be differentially regulated in GF conditions. In order to test this hypothesis, we assessed the response to DSS in conventional mice, GF mice, and conventional animals with acquired depletion of the microbiota [which we will refer to as 'pseudo-GF' or PGF here].…”

Section: Introductionmentioning

confidence: 99%

Germ-free and Antibiotic-treated Mice are Highly Susceptible to Epithelial Injury in DSS Colitis

Hernández‐Chirlaque

Aranda

Ocón

et al. 2016

ECCOJC

217

137

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Intravenous Injection of Endogenous Microbial Components Abrogates DSS-Induced Colitis

Abstract: Pretreatment with high amount of endogenous bacterial components has a profound tolerogenic effect on the systemic and mucosal immune responses resulting in reduced intestinal inflammation and abrogates colitis-induced weight loss.

Cited by 9 publications

References 41 publications

Opposite Role of Tumor Necrosis Factor Receptors in Dextran Sulfate Sodium-Induced Colitis in Mice

Opposite Role of Tumor Necrosis Factor Receptors in Dextran Sulfate Sodium-Induced Colitis in Mice

Protective role of tumor necrosis factor (TNF) receptors in chronic intestinal inflammation: TNFR1 ablation boosts systemic inflammatory response

Germ-free and Antibiotic-treated Mice are Highly Susceptible to Epithelial Injury in DSS Colitis

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