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IN THIS ISSUE
A link between impaired intestinal permeability and inflammatory intestinal disease
Disease Models & Mechanisms 2015 8: e0802
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Impaired intestinal barrier function is thought to be a common major factor in food hypersensitivity, inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), and colitis-associated cancer (CAC). Joan Heath and colleagues found that Gpa33–/– mice, which do not express the intestinal epithelium-specific cell surface glycoprotein A33 (GPA33), exhibited increased intestinal permeability and hypersensitivity to food antigens. Such alterations worsened upon exposure to dextran sodium sulphate (DSS), an intestinal luminal irritant, and led to the development of colitis in Gpa33–/– mice. Prior administration of azoxymethane (AOM; a colon-specific mutagen) induced CAC in DSS-treated Gpa33–/– mice but not in Gpa33–/– mice treated with AOM alone. Interestingly, human gene expression data showed that GPA33 RNA expression is reduced in the inflamed bowel of CD- and UC-affected individuals. Collectively, these data suggest a role for GPA33 in intestinal barrier function, which influences susceptibility to inflammatory intestinal pathologies. Gpa33–/– mice could be used to test the restoration of barrier function as a strategy to treat and prevent such pathologies. Page 805

Figure1
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This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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DMM and COVID-19

We are aware that the COVID-19 pandemic is having an unprecedented impact on researchers worldwide. The Editors of all The Company of Biologists’ journals have been considering ways in which we can alleviate concerns that members of our community may have around publishing activities during this time. Read about the actions we are taking at this time.

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Monica Justice bids farewell to DMM

In her farewell Editorial, outgoing Editor-in-Chief Monica Justice reminds us of the past half-decade of growth and of DMM's commitment to support the disease modelling community, concluding, “The knowledge and experience I gained during my time as Senior Editor and EiC at DMM is invaluable: working within a not-for-profit community publishing environment is a joy.”


3D imaging of beta cell mass in diabetic mouse models

In their inducible mouse model of diabetes, Roostalu et al. demonstrate how quantitative light-sheet imaging can capture changes in individual islets to help pharmacological research in diabetes.

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Modelling Joubert syndrome patient-derived mutations in C. elegans

In this issue’s Editor’s choice, Karen Lange and colleagues used C. elegans to model and characterise two patient-derived mutations that cause the ciliopathy Joubert syndrome.


Interview – Karen Lange

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