变形链球菌
病变
医学
细胞外基质
抗体
牙周病原体
细胞外
基因剔除小鼠
微生物学
牙周炎
病理
生物
免疫学
内科学
细菌
受体
牙龈卟啉单胞菌
细胞生物学
遗传学
作者
Yuri Taniguchi,Kazuhisa Ouhara,Masae Kitagawa,Keiichi Akutagawa,Miki Kawada-Matsuo,Tetsuya Tamura,Ruoqi Zhai,Yuta Hamamoto,Mikihito Kajiya,Shinji Matsuda,Hirofumi Maruyama,Hitoshi Komatsuzawa,Hideki Shiba,Noriyoshi Mizuno
摘要
Cerebral hemorrhage severely affects the daily life of affected individuals. Streptococcus mutans and its adhesion factor Cnm increase the adverse effects of cerebral hemorrhages. However, the mechanism by which Cnm-positive bacteria migrate from apical lesions to cerebral hemorrhage sites is unclear. Therefore, we established an S. mutans-infected apical lesion in a rat model of hypertension and investigated the neurological symptoms associated with cerebral hemorrhage. Eighteen 12-week-old stroke-prone spontaneously hypertensive rats were randomly divided into three groups, i.e. the no infection (control), dental infection with S. mutans KSM153 wild type (Cnm positive), and KSM153 Δcnm groups. Immunofluorescent staining was performed to visualize S. mutans protein. Serum interleukin-1β levels were measured. The adhesion of S. mutans to the extracellular matrix and human fibroblast cells was also analyzed. Serum antibody titers against S. mutans were comparable between Cnm positive and knockout mutants. However, 3-10 days post-infection, neurological symptom scores and cerebral hemorrhage scores were higher in Cnm-positive rats than in knockout mutants. The localization of S. mutans-derived protein was observed in the vicinity of disrupted blood vessels. Serum interleukin-1β levels significantly increased post-KSM153 WT infection. Cnm-positive S. mutans clinical isolates showed increased adhesion to the extracellular matrix, human dental pulp cells, and human umbilical vein endothelial cells compared with the Cnm-negative S. mutans isolates. In conclusion, Cnm-positive bacteria colonize the apical lesion site using the extracellular matrix as a foothold and affect cerebral hemorrhage via the bloodstream.
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