Seo Yoojin, Oh Su-Jeong, Ahn Ji-Su, Shin Ye Young, Yang Ji Won, Kim Hyung-Sik
1Department of Life Science in Dentistry, School of Dentistry, Pusan National University, Busandaehak-ro 49, Yangsan, 50612 Republic of Korea.
2Dental and Life Science Institute, Pusan National University, Yangsan, 50612 Republic of Korea.
Lab Anim Res. 2019 Dec 4;35:26. doi: 10.1186/s42826-019-0029-6. eCollection 2019.
Emerging evidences have reported that periodontitis can be a risk factor for the pathogenesis of various systemic diseases. (), one of the crucial pathogens in chronic periodontitis, has been spotlighted as a potential cause for the promotion and acceleration of periodontitis-associated systemic disorders. To investigate the association between and intestinal disease or homeostasis, we treated -derived lipopolysaccharide (LPS) in murine colitis model or intestinal organoid, respectively. -derived LPS ( LPS) was administrated into chemically induced murine colitis model and disease symptoms were monitored compared with the infusion of LPS derived from ( LPS). Organoids isolated and cultured from mouse small intestine were treated with or LPS and further analyzed for the generation and composition of organoids. In vivo observations demonstrated that both and LPS exerted slight protective effects against murine colitis. LPS did not affect the generation and growth of intestinal epithelial organoids. Among subtypes of epithelial cells, markers for stem cells, goblet cells or Paneth cells were changed in response to LPS. Taken together, these results indicate that LPS leads to partial improvement in colitis and that its treatment does not significantly affect the self-organization of intestinal organoids but may regulate the epithelial composition.
新出现的证据表明，牙周炎可能是多种全身性疾病发病机制的一个风险因素。（某种细菌）作为慢性牙周炎的关键病原体之一，已成为牙周炎相关全身性疾病进展和加速的潜在原因而备受关注。为了研究（该细菌）与肠道疾病或内环境稳态之间的关联，我们分别在小鼠结肠炎模型或肠道类器官中用（该细菌）衍生的脂多糖（LPS）进行处理。将（该细菌）衍生的LPS（即[细菌名称]LPS）注入化学诱导的小鼠结肠炎模型中，并与注入（另一种细菌）衍生的LPS（即[另一种细菌]LPS）相比，监测疾病症状。从小鼠小肠分离并培养的类器官用（该细菌）或（另一种细菌）LPS进行处理，并进一步分析类器官的生成和组成。体内观察结果表明，（该细菌）LPS和（另一种细菌）LPS对小鼠结肠炎均有轻微的保护作用。（该细菌）LPS不影响肠道上皮类器官的生成和生长。在上皮细胞亚型中，干细胞、杯状细胞或潘氏细胞的标志物因（该细菌）LPS而发生变化。综上所述，这些结果表明，（该细菌）LPS可使结肠炎部分改善，其处理不会显著影响肠道类器官的自我组织，但可能会调节上皮组成。
