CCDC88B is required for pathogenesis of inflammatory bowel disease

Nassima Fodil (), Neda Moradin, Vicki Leung, Jean-Frederic Olivier, Irena Radovanovic, Thiviya Jeyakumar, Manuel Flores Molina, Ashley McFarquhar, Romain Cayrol, Dominique Bozec, Naglaa H. Shoukry, Michiaki Kubo, Julia Dimitrieva, Edouard Louis, Emilie Theatre, Stephanie Dahan, Yukihide Momozawa, Michel Georges, Garabet Yeretssian and Philippe Gros ()
Additional contact information
Nassima Fodil: McGill Center for the Study of Complex Traits, Department of Human Genetics, Department of Biochemistry, McGill University, 3649 Sir William Osler Promenade
Neda Moradin: McGill Center for the Study of Complex Traits, Department of Human Genetics, Department of Biochemistry, McGill University, 3649 Sir William Osler Promenade
Vicki Leung: McGill Center for the Study of Complex Traits, Department of Human Genetics, Department of Biochemistry, McGill University, 3649 Sir William Osler Promenade
Jean-Frederic Olivier: McGill Center for the Study of Complex Traits, Department of Human Genetics, Department of Biochemistry, McGill University, 3649 Sir William Osler Promenade
Irena Radovanovic: McGill Center for the Study of Complex Traits, Department of Human Genetics, Department of Biochemistry, McGill University, 3649 Sir William Osler Promenade
Thiviya Jeyakumar: McGill Center for the Study of Complex Traits, Department of Human Genetics, Department of Biochemistry, McGill University, 3649 Sir William Osler Promenade
Manuel Flores Molina: Centre de Recherche du Centre Hospitalier de l’Université de Montréal (CRCHUM), 900, Saint Denis Street, Pavillion R
Ashley McFarquhar: McGill Center for the Study of Complex Traits, Department of Human Genetics, Department of Biochemistry, McGill University, 3649 Sir William Osler Promenade
Romain Cayrol: Département de Pathologie et de Biologie Cellulaire de l’Université de Montréal, C.P. 6128, succ. Centre-ville
Dominique Bozec: Immunology Institute, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai
Naglaa H. Shoukry: Centre de Recherche du Centre Hospitalier de l’Université de Montréal (CRCHUM), 900, Saint Denis Street, Pavillion R
Michiaki Kubo: Laboratory for Genotyping Development, Center for Integrative Medical Sciences, RIKEN 1-7-22 Suehiro-cho, Tsurumi-ku
Julia Dimitrieva: Unit of Animal Genomics, GIGA-R and Faculty of Veterinary Medicine, Universite de Liège (B34), avenue de l’Hôpital 1
Edouard Louis: Unit of Animal Genomics, GIGA-R and Faculty of Veterinary Medicine, Universite de Liège (B34), avenue de l’Hôpital 1
Emilie Theatre: Unit of Animal Genomics, GIGA-R and Faculty of Veterinary Medicine, Universite de Liège (B34), avenue de l’Hôpital 1
Stephanie Dahan: Immunology Institute, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai
Yukihide Momozawa: Laboratory for Genotyping Development, Center for Integrative Medical Sciences, RIKEN 1-7-22 Suehiro-cho, Tsurumi-ku
Michel Georges: Unit of Animal Genomics, GIGA-R and Faculty of Veterinary Medicine, Universite de Liège (B34), avenue de l’Hôpital 1
Garabet Yeretssian: Immunology Institute, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai
Philippe Gros: McGill Center for the Study of Complex Traits, Department of Human Genetics, Department of Biochemistry, McGill University, 3649 Sir William Osler Promenade

Nature Communications, 2017, vol. 8, issue 1, 1-12

Abstract: Abstract Inflammatory bowel disease (IBD) involves interaction between host genetic factors and environmental triggers. CCDC88B maps within one IBD risk locus on human chromosome 11q13. Here we show that CCDC88B protein increases in the colon during intestinal injury, concomitant with an influx of CCDC88B+lymphoid and myeloid cells. Loss of Ccdc88b protects against DSS-induced colitis, with fewer pathological lesions and reduced intestinal inflammation in Ccdc88b-deficient mice. In a T cell transfer model of colitis, Ccdc88b mutant CD4+ T cells do not induce colitis in immunocompromised hosts. Expression of human CCDC88B RNA and protein is higher in IBD patient colons than in control colon tissue. In human CD14+ myeloid cells, CCDC88B is regulated by cis-acting variants. In a cohort of patients with Crohn’s disease, CCDC88B expression correlates positively with disease risk. These findings suggest that CCDC88B has a critical function in colon inflammation and the pathogenesis of IBD.

Date: 2017
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DOI: 10.1038/s41467-017-01381-y

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