Inflammatory bowel diseases · 2025
Ulcerative Colitis Aggravates Periodontitis via Inducing Myelopoiesis.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Kuang Xinyi, Jia Xiaoyue, Peng Xian, Zheng Xin, Zhao Lei, Xie Jing, Zheng Liwei, Xu Xin
Аннотация
OBJECTIVES: The intercorrelations between periodontitis and inflammatory bowel disease have been recognized for years. Accumulating evidence has shown that patients with ulcerative colitis (UC) have a higher prevalence and severity of periodontitis. However, the underlying mechanisms by which UC aggravates periodontal destruction are still unclear.
METHODS: Multiple murine models, including DSS-induced colitis (DIC)/ligature-induced periodontitis (LIP), DIC/LIP rescued by berberine, and LIP after DIC remission models were established to investigate the mechanisms by which UC exacerbates periodontal inflammation.
RESULTS: DIC mice exhibited a disrupted intestinal barrier with dysbiotic gut microbiota, corroborating the elevated serum levels of LPS and IL-1. Compared to DIC-free/LIP mice, DIC/LIP mice showed aggravated alveolar bone resorption, with enrichment of neutrophil extracellular traps (NETs) in periodontal tissues. DIC promoted myelopoiesis of hematopoietic stem and progenitor cells (HSPCs) by up-regulating the myeloid differentiation pathway. Intragastric administration of berberine dampened DIC and rescued the myeloid skewing of HSPCs, consequently alleviating periodontal destruction. Intriguingly, LIP induction after DIC remission still exhibited aggravated periodontal destruction and myeloid skewing of HSPCs, indicating a UC-trained immunity against periodontal damage.
CONCLUSIONS: Increased gut permeability and microbial dysbiosis in UC elevate the serum level of LPS and IL-1, inducing myeloid skewing of HSPCs with an immune memory. Generation of inflammatory potential myeloid cells causes NETs accumulation and aggravates periodontal destruction in the UC-related periodontitis.
METHODS: Multiple murine models, including DSS-induced colitis (DIC)/ligature-induced periodontitis (LIP), DIC/LIP rescued by berberine, and LIP after DIC remission models were established to investigate the mechanisms by which UC exacerbates periodontal inflammation.
RESULTS: DIC mice exhibited a disrupted intestinal barrier with dysbiotic gut microbiota, corroborating the elevated serum levels of LPS and IL-1. Compared to DIC-free/LIP mice, DIC/LIP mice showed aggravated alveolar bone resorption, with enrichment of neutrophil extracellular traps (NETs) in periodontal tissues. DIC promoted myelopoiesis of hematopoietic stem and progenitor cells (HSPCs) by up-regulating the myeloid differentiation pathway. Intragastric administration of berberine dampened DIC and rescued the myeloid skewing of HSPCs, consequently alleviating periodontal destruction. Intriguingly, LIP induction after DIC remission still exhibited aggravated periodontal destruction and myeloid skewing of HSPCs, indicating a UC-trained immunity against periodontal damage.
CONCLUSIONS: Increased gut permeability and microbial dysbiosis in UC elevate the serum level of LPS and IL-1, inducing myeloid skewing of HSPCs with an immune memory. Generation of inflammatory potential myeloid cells causes NETs accumulation and aggravates periodontal destruction in the UC-related periodontitis.