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WNT2B Deficiency Causes Enhanced Susceptibility to Colitis Due to Increased Inflammatory Cytokine Production. 2024
Amy E O'Connell, and
Sathuwarman Raveenthiraraj, and
Luiz Fernando Silva Oliveira, and
Comfort Adegboye, and
Venkata Siva Dasuri, and
Wanshu Qi, and
Radhika S Khetani, and
Akaljot Singh, and
Nambirajam Sundaram, and
Jasmine Lin, and
Prathima Nandivada, and
Lorena Rincón-Cruz, and
Jeffrey D Goldsmith, and
Jay R Thiagarajah, and
Diana L Carlone, and
Jerrold R Turner, and
Pankaj B Agrawal, and
Michael Helmrath, and
David T Breault
Division of Newborn Medicine; The Manton Center for Orphan Disease Research at Boston Children's Hospital, Boston, MA;; Department of Pediatrics, Harvard Medical School, Boston, MA;. Electronic address: amy.oconnell@childrens.harvard.edu.
OBJECTIVE Humans with WNT2B deficiency have severe intestinal disease, including significant inflammatory injury, highlighting a critical role for WNT2B. We sought to understand how WNT2B contributes to intestinal homeostasis. METHODS We investigated the intestinal health of Wnt2b knock out (KO) mice. We assessed the baseline histology and health of the small intestine and colon, as well as the impact of inflammatory challenge using dextran sodium sulfate (DSS). We also evaluated human intestinal tissue. RESULTS Mice with WNT2B deficiency had normal baseline histology but enhanced susceptibility to DSS colitis due to an increased early injury response. While ISC markers were decreased, epithelial proliferation was similar to controls. Wnt2b KO mice showed an enhanced inflammatory signature after DSS treatment. Wnt2b KO colon and human WNT2B-deficient organoids both had increased levels of CXCR4 and IL6, and biopsy tissue from humans showed increased neutrophils. CONCLUSIONS WNT2B is important for regulation of inflammation in the intestine. Absence of WNT2B leads to increased expression of inflammatory cytokines and increased susceptibility to gastrointestinal inflammation, particularly in the colon.
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