Upregulation of complement C1q reflects mucosal regeneration in a mouse model of colitis
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ORIGINAL PAPER
Upregulation of complement C1q reflects mucosal regeneration in a mouse model of colitis Naohiko Gunji1 · Kyoko Katakura1 · Kazumichi Abe1 · Kazumasa Kawashima1 · Tatsuo Fujiwara1 · Michio Onizawa1 · Atsushi Takahashi1 · Hiromasa Ohira1 Received: 15 January 2020 / Accepted: 18 September 2020 © The Japanese Society for Clinical Molecular Morphology 2020
Abstract Confirming mucosal healing is important in inflammatory bowel disease treatment. Complement C1q-mediated Wnt signaling activation has recently been suggested to mediate tissue repair and mucosal regeneration. We investigated the involvement of complement C1q and Wnt signaling in intestinal mucosal regeneration using a murine colitis model. The colitis model was established by providing C57BL/6J mice with 4% dextran sodium sulfate (DSS) for 1 week (inflammation phase) followed by regular water for 2 weeks (recovery phase). After 3 weeks, we investigated the relationship between C1q in serum and colonic tissue during the inflammation and recovery phases. We assessed Wnt signaling activity by evaluating β-catenin expression in mouse intestinal tissue. Serum C1q levels were elevated during the recovery phase. C1q-specific staining indicated high C1q expression in pathological intestinal tissue during the inflammation and recovery phases. C1q mRNA and protein expression was increased during both phases. Interestingly, C1q-expressing cells were consistent with macrophages (F4/80-positive cells). Moreover, the expression of β-catenin increased in the colonic tissues during the recovery phase of DSS-induced colitis but decreased during the inflammation phase of DSS-induced colitis. C1q expression may mediate Wnt signaling activity and intestinal epithelial regeneration. Keywords Inflammatory bowel disease · C1q · Wnt signaling · β-catenin · Lgr5
Introduction Inflammatory bowel disease (IBD) is a multifactorial disease that involves multiple genetic and environmental factors and abnormal immune responses. Confirming the regeneration and healing of the intestinal mucosa (mucosal healing) using endoscopy is necessary to determine whether IBD treatment has been successful in daily practice. Critically, recent reports have emphasized the importance of mucosal healing, as failure of mucosal healing is a major predictor of clinical recurrence [1, 2]. Endoscopy is the best modality to diagnose and monitor the mucosal status of IBD patients, but it frequently cannot be performed because of the cost, invasiveness, and potential risk of disease exacerbation. Alternatively, less expensive * Kazumichi Abe k‑[email protected] 1
Department of Gastroenterology, Fukushima Medical University School of Medicine, 1 Hikarigaoka, Fukushima City, Fukushima 960‑1295, Japan
and less invasive serum biomarkers such as C-reactive protein (CRP) and the erythrocyte sedimentation rate (ESR) are also used to monitor inflammatory activity [3]. However, these markers do not always correlate with disease activity in IBD. More recently, research efforts have been directed towards t
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