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Bcl-3 deficiency protects against dextran-sodium sulphate-induced colitis in the mouse

Overview of attention for article published in Clinical & Experimental Immunology, July 2013
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  • Above-average Attention Score compared to outputs of the same age and source (54th percentile)

Mentioned by

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5 tweeters

Citations

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19 Dimensions

Readers on

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27 Mendeley
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Title
Bcl-3 deficiency protects against dextran-sodium sulphate-induced colitis in the mouse
Published in
Clinical & Experimental Immunology, July 2013
DOI 10.1111/cei.12119
Pubmed ID
Authors

C O'Carroll, G Moloney, G Hurley, S Melgar, E Brint, K Nally, R J Nibbs, F Shanahan, R J Carmody

Abstract

Bcl-3 is a member of the IκB family of proteins and is an essential negative regulator of Toll-like receptor-induced responses. Recently, a single nucleotide polymorphism associated with reduced Bcl-3 gene expression has been identified as a potential risk factor for Crohn's disease. Here we report that in contrast to the predictions of single nucleotide polymorphism (SNP) analysis, patients with Crohn's disease and ulcerative colitis demonstrate elevated Bcl-3 mRNA expression relative to healthy individuals. To explore further the potential role of Bcl-3 in inflammatory bowel disease (IBD), we used the dextran-sodium sulphate (DSS)-induced model of colitis in Bcl-3(-/-) mice. We found that Bcl-3(-/-) mice were less sensitive to DSS-induced colitis compared to wild-type controls and demonstrated no significant weight loss following treatment. Histological analysis revealed similar levels of oedema and leucocyte infiltration between DSS-treated wild-type and Bcl-3(-/-) mice, but showed that Bcl-3(-/-) mice retained colonic tissue architecture which was absent in wild-type mice following DSS treatment. Analysis of the expression of the proinflammatory cytokines interleukin (IL)-1β, tumour necrosis factor (TNF)-α and IL-6 revealed no significant differences between DSS-treated Bcl-3(-/-) and wild-type mice. Analysis of intestinal epithelial cell proliferation revealed enhanced proliferation in Bcl-3(-/-) mice, which correlated with preserved tissue architecture. Our results reveal that Bcl-3 has an important role in regulating intestinal epithelial cell proliferation and sensitivity to DSS-induced colitis which is distinct from its role as a negative regulator of inflammation.

Twitter Demographics

The data shown below were collected from the profiles of 5 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 27 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Russia 1 4%
Unknown 26 96%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 10 37%
Researcher 5 19%
Student > Bachelor 3 11%
Librarian 1 4%
Student > Master 1 4%
Other 1 4%
Unknown 6 22%
Readers by discipline Count As %
Medicine and Dentistry 6 22%
Biochemistry, Genetics and Molecular Biology 4 15%
Agricultural and Biological Sciences 4 15%
Immunology and Microbiology 2 7%
Psychology 2 7%
Other 1 4%
Unknown 8 30%

Attention Score in Context

This research output has an Altmetric Attention Score of 2. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 25 April 2013.
All research outputs
#11,946,097
of 19,800,203 outputs
Outputs from Clinical & Experimental Immunology
#2,517
of 3,529 outputs
Outputs of similar age
#90,574
of 170,182 outputs
Outputs of similar age from Clinical & Experimental Immunology
#19
of 44 outputs
Altmetric has tracked 19,800,203 research outputs across all sources so far. This one is in the 38th percentile – i.e., 38% of other outputs scored the same or lower than it.
So far Altmetric has tracked 3,529 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.1. This one is in the 27th percentile – i.e., 27% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 170,182 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 45th percentile – i.e., 45% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 44 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 54% of its contemporaries.