The role of eosinophils in inflammatory bowel disease

Al-Haddad, Sahar; Riddell, R H

doi:10.1136/gut.2005.072595

Cited by 77 publications

(68 citation statements)

References 30 publications

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“…Interestingly, the differences in allele frequencies were found in populations with IBD but not in patients with celiac disease, rheumatoid arthritis, or type 1 diabetes. Eosinophilia, such as we observed in Ndfip1−/− mice, is frequently observed in patients in IBD, 22,23 especially in the earlier phases of disease development. However, other aspects of the pathology associated with IBD are not reproduced in our mice.…”

Section: Discussionsupporting

confidence: 61%

The ubiquitin ligase adaptor Ndfip1 regulates T cell-mediated gastrointestinal inflammation and inflammatory bowel disease susceptibility

Ramón

Riling

Bradfield³

et al. 2011

Mucosal Immunology

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Nedd4 family interacting protein 1 (Ndfip1) is an adaptor protein that regulates Itch, an E3 ubiquitin ligase that ubiquitylates JunB, thereby preventing interleukin (IL)-4 and IL-5 production. Mice lacking Ndfip1 or Itch develop T helper type 2 (TH2)-mediated inflammation in the skin and lungs and die prematurely. In this study we show that Ndfip1 − / − mice also develop inflammation in the gastrointestinal tract. Inflammation is characterized by infiltration of eosinophils and T cells and is accompanied by a failure to gain weight. T cells are both necessary and sufficient for eosinophil recruitment and inflammation. This is because Ndfip1 − / − T cells become activated and produce IL-5. Itch mutant mice develop much less severe gastrointestinal inflammation, suggesting that Ndfip1 regulation of Itch cannot entirely account for this phenotype and that Ndfip1 has both Itch-dependent and Itch-independent roles. Ndfip1 may also regulate human disease. We found single-nucleotide polymorphisms in the Ndfip1 locus that associate with inflammatory bowel disease. Taken together, our data support a role for Ndfip1 in gastrointestinal inflammation in both mice and humans.

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Section: Discussionsupporting

confidence: 61%

The ubiquitin ligase adaptor Ndfip1 regulates T cell-mediated gastrointestinal inflammation and inflammatory bowel disease susceptibility

Ramón

Riling

Bradfield³

et al. 2011

Mucosal Immunology

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“…They are recruited by chemokines that act on CCR3, especially eotaxin, and are able to secrete toxic inflammatory mediators, such as EPO, which is stored within vesicles (Al-Haddad & Riddell, 2005;Woodruff et al, 2011). Eosinophils are thought to play a major pro-inflammatory role in IBD and contribute to diarrhoea, tissue destruction and fibrosis formation (Vieira et al, 2009;Albert et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

“…Eosinophils are thought to play a role in the pathogenesis of IBD (Al-Haddad & Riddell, 2005). High levels of EPO activity quantified in the colon of DSS-treated animals suggested an increased influx of eosinophils in this organ (Fig.…”

Section: Ecn Treatment Modulates the Host Immune Response After Dss-imentioning

confidence: 99%

Escherichia coli strain Nissle 1917 ameliorates experimental colitis by modulating intestinal permeability, the inflammatory response and clinical signs in a faecal transplantation model

Souza

Elian

Paula

et al. 2016

Journal of Medical Microbiology

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Inflammatory bowel diseases (IBDs) are a group of inflammatory conditions of the gut that include ulcerative colitis and Crohn's disease. Probiotics are live micro-organisms that may be used as adjuvant therapy for patients with IBD. The aim of this study was to evaluate the effect of prophylactic ingestion of Escherichia coli strain Nissle 1917 (EcN) in a murine model of colitis. For induction of colitis, mice were given a 3.5 % dextran sodium sulfate (DSS) solution for 7 days in drinking water. EcN administration to mice subjected to DSS-induced colitis resulted in significant reduction in clinical and histopathological signs of disease and preservation of intestinal permeability. We observed reduced inflammation, as assessed by reduced levels of neutrophils, eosinophils, chemokines and cytokines. We observed an increase in the number of regulatory T-cells in Peyer's patches. Germ-free mice received faecal content from control or EcN-treated mice and were then subjected to DSS-induced colitis. We observed protection from colitis in animals that were colonized with faecal content from EcNtreated mice. These results suggest that preventative oral administration of EcN or faecal microbiota transplantation with EcN-containing microbiota ameliorates DSS-induced colitis by modifying inflammatory responsiveness to DSS.

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“…Eosinophils are found in excess in IBD, where they are postulated to modulate both tissue injury and repair [5]. Eosinophils originate in the bone marrow and migrate predominantly to the gastrointestinal tract under the influence of interleukin-5 and the eotaxin chemokines, all of which are overexpressed in IBD [6,7].…”

Section: Introductionmentioning

confidence: 99%

Recurrent Blood Eosinophilia in Ulcerative Colitis Is Associated with Severe Disease and Primary Sclerosing Cholangitis

et al. 2012

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Background and Aims Eosinophils are implicated in the pathogenesis of inflammatory bowel disease (IBD). A subset of IBD patients develops blood eosinophilia and the clinical profile of these patients is undefined. We sought to characterize IBD patients with and without eosinophilia. Methods We studied a prospective registry of 1176 IBD patients followed in a tertiary referral center. Patients who developed eosinophilia at any time were identified by electronic medical record query. We performed a chart review case-control study comparing patients with recurrent eosinophilia versus randomly selected disease matched patients with no history of eosinophilia. Histological analysis was performed on selected cases and controls. Results Eosinophilia at any time was more prevalent in ulcerative colitis (UC) patients than Crohn’s disease patients (22.2% vs. 12.7%), as was recurrent eosinophilia (3.4% vs. 0.7%). UC patients with recurrent eosinophilia were predominantly male compared to the control UC population (81.3% vs. 46.9%) and had higher rates of colectomy for either medically refractory disease or dysplasia/cancer than control UC patients (56.3% vs. 15.6%). Primary sclerosing cholangitis (PSC) occurred in 37.5% of UC patients with recurrent eosinophilia compared to only 3.1% in the UC controls. Histological analysis of random diagnostic samples from UC patients with recurrent eosinophilia demonstrated a normal eosinophil pattern as seen in the control UC population. Conclusions Eosinophilia-associated UC is a subgroup of IBD associated with severe colitis and PSC. Further studies are warranted to characterize molecular mechanisms underlying eosinophilia-associated UC and to determine optimal approaches for therapy.

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The role of eosinophils in inflammatory bowel disease

Abstract: Wireless pH monitoring is a significant advance for intraluminal pH recording. It will provide more meaningful data for evaluation of patients and, hopefully, more discriminative diagnosis

Cited by 77 publications

References 30 publications

The ubiquitin ligase adaptor Ndfip1 regulates T cell-mediated gastrointestinal inflammation and inflammatory bowel disease susceptibility

The ubiquitin ligase adaptor Ndfip1 regulates T cell-mediated gastrointestinal inflammation and inflammatory bowel disease susceptibility

Escherichia coli strain Nissle 1917 ameliorates experimental colitis by modulating intestinal permeability, the inflammatory response and clinical signs in a faecal transplantation model

Recurrent Blood Eosinophilia in Ulcerative Colitis Is Associated with Severe Disease and Primary Sclerosing Cholangitis

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