Inflammatory bowel diseases · 2025
Serum Periostin is Able to Stratify Type 2-Dominant Ulcerative Colitis.
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Takedomi Hironobu, Nunomura Satoshi, Nanri Yasuhiro, Honda Yuko, Yokomizo Kanako, Akutagawa Takashi, Tsuruoka Nanae, Sakata Yasuhisa, Conway Simon, Kawaguchi Atsushi, Aishima Shinichi, Esaki Motohiro, Izuhara Kenji
Аннотация
BACKGROUND: Ulcerative colitis (UC) is a heterogeneous disease composed of different endotypes. It is important to develop useful biomarkers for endotyping UC; however, available biomarkers are insufficient. We have already established that periostin is a surrogate biomarker of type 2 inflammation. In this study, we examined the usefulness of periostin as a biomarker of UC and the role of periostin in its pathogenesis.
METHODS: We examined periostin expression in the colons of UC patients. We next investigated serum periostin in UC patients and its correlation with eosinophilic infiltration in their colons. We then examined whether serum periostin could predict the efficacy of oral prednisolone. Finally, we investigated the role of periostin in UC pathogenesis by creating its genetic deficiency using dextran sulfate sodium (DSS)-treated mice.
RESULTS: Periostin expression and serum periostin were significantly high in UC patients compared to healthy controls; however, both were diverse, showing heterogeneity of the underlying mechanism of UC. Both serum periostin and tissue periostin expression, but not blood eosinophils, were significantly associated with eosinophil infiltration. Type 2-dominant UC patients as defined by serum periostin showed significantly higher clinical remission rates for the treatment with oral prednisolone. Genetic deficiency in periostin improved colonic inflammation in a DSS-treated mouse model.
CONCLUSIONS: Periostin can be a useful biomarker to stratify type 2-dominant UC patients, thereby predicting the efficacy of oral prednisolone. Moreover, periostin plays an important role in the setting of type 2-dominant UC.
METHODS: We examined periostin expression in the colons of UC patients. We next investigated serum periostin in UC patients and its correlation with eosinophilic infiltration in their colons. We then examined whether serum periostin could predict the efficacy of oral prednisolone. Finally, we investigated the role of periostin in UC pathogenesis by creating its genetic deficiency using dextran sulfate sodium (DSS)-treated mice.
RESULTS: Periostin expression and serum periostin were significantly high in UC patients compared to healthy controls; however, both were diverse, showing heterogeneity of the underlying mechanism of UC. Both serum periostin and tissue periostin expression, but not blood eosinophils, were significantly associated with eosinophil infiltration. Type 2-dominant UC patients as defined by serum periostin showed significantly higher clinical remission rates for the treatment with oral prednisolone. Genetic deficiency in periostin improved colonic inflammation in a DSS-treated mouse model.
CONCLUSIONS: Periostin can be a useful biomarker to stratify type 2-dominant UC patients, thereby predicting the efficacy of oral prednisolone. Moreover, periostin plays an important role in the setting of type 2-dominant UC.