Oral Infection Promote T Helper 17/Treg Imbalance in the Development of Atherosclerosis
Overview
Affiliations
Background/purpose: Increasing studies have indicated the involvement of in atherosclerosis. T helper 17 (Th17)/Treg balance is critical during atherosclerosis. However, whether oral infection is associated with Th17/Treg imbalance is unclear. The aim of the present study was to investigate the effect of on Th17/Treg balance during atherosclerosis.
Materials And Methods: ApoE and C57BL/6 mice were inoculated orally with 33277 for 9 weeks. The alveolar bone loss was assessed by microcomputerized tomography. The area of atherosclerosis plaque was identified by oil red O staining. Plaque stability was analyzed by CD68 and αSMA immunohistochemistry staining and Masson staining. The frequency of Th17 and Treg in spleen was detected by flow cytometry. The mRNA expression of Th17- and Treg-related factors was determined by quantitative polymerase chain reaction. Interleukin (IL)-6, a critical factor in modulating T-cell differentiation, was determined from spleen cells and mouse dendritic cells by enzyme-linked immunosorbent assay.
Results: Long-term oral infection induced alveolar bone resorption. In ApoE mice, enhanced atherosclerotic lesion formation and plaque instability accompanied with a decreased Treg frequency and an increased Th17 cell frequency. In addition, mRNA expression of retinoic acid receptor-related orphan receptor γt and IL-17 was increased, and that of transforming growth factor (TGF) β and IL-10 was decreased in -infected ApoE mice. Furthermore, secretion of IL-6 was elevated in the spleen of -infected ApoE mice, as well as in mouse dendritic cells after infection.
Conclusion: oral infection may promote Th17/Treg imbalance by influencing T-cell differentiation during the process of atherosclerosis, with a larger lesion area and decreasing plaque instability.
Bacterial signature in retrieved thrombi of patients with acute ischemic stroke-a systematic review.
Zarrintan A, Ghozy S, Thirupathi K, Walden K, Brinjikji W, Kallmes D Ther Adv Neurol Disord. 2024; 17:17562864241296713.
PMID: 39525877 PMC: 11550500. DOI: 10.1177/17562864241296713.
Zhu K, Wang L, Xiao Y, Zhang X, You G, Chen Y J Nanobiotechnology. 2024; 22(1):336.
PMID: 38880905 PMC: 11180412. DOI: 10.1186/s12951-024-02606-1.
Periodontitis in ischemic stroke: impact of on thrombus composition and ischemic stroke outcomes.
Freiherr Von Seckendorff A, Solo Nomenjanahary M, Labreuche J, Ollivier V, Di Meglio L, Dupont S Res Pract Thromb Haemost. 2024; 8(1):102313.
PMID: 38318152 PMC: 10840352. DOI: 10.1016/j.rpth.2023.102313.
The Roles of Periodontal Bacteria in Atherosclerosis.
Huang X, Xie M, Lu X, Mei F, Song W, Liu Y Int J Mol Sci. 2023; 24(16).
PMID: 37629042 PMC: 10454115. DOI: 10.3390/ijms241612861.
regulates atherosclerosis through an immune pathway.
Ruan Q, Guan P, Qi W, Li J, Xi M, Xiao L Front Immunol. 2023; 14:1103592.
PMID: 36999040 PMC: 10043234. DOI: 10.3389/fimmu.2023.1103592.