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依那西普可预防 FcγRIIb-/- 狼疮模型中 TNF-α 介导的下颌骨丢失。

Etanercept prevents TNF-α mediated mandibular bone loss in FcγRIIb-/- lupus model.

机构信息

Skeletal Disorders Research Unit, Department of Physiology, Faculty of Dentistry, Chulalongkorn University, Bangkok, Thailand.

Interdisciplinary Program of Biomedical Sciences, Graduate School, Chulalongkorn University, Bangkok, Thailand.

出版信息

PLoS One. 2021 Apr 16;16(4):e0250215. doi: 10.1371/journal.pone.0250215. eCollection 2021.

DOI:10.1371/journal.pone.0250215
PMID:33861790
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8051757/
Abstract

Patients with systemic lupus erythematosus are at increased risk for alveolar bone loss due to periodontitis possibly as a result of a pathogenic immune response to oral bacteria and inflammation. The aim of the present study was to investigate whether an anti-TNF-α antagonist could prevent mandibular bone loss in the FcγRIIb-/- mouse model of lupus. Mice lacking FcγRIIb had decreased cancellous and cortical bone volume at 6 months of age. Etanercept increased cancellous but not cortical bone volume in WT and increased both cancellous bone volume and cortical thickness in FcγRIIb-deficient mice. FcγRIIb deficiency decreased mRNA levels for osteoblast marker genes, Osx, Col1a1 and Alp without any change in osteoclast marker genes. Etanercept increased Osx, Alp, and Ocn in both WT and FcγRIIb-/- mice. Osteoclast marker genes including TNF-α, Trap and RANKL/OPG ratio was decreased in WT. Serum markers of proinflammatory cytokines, TNF-α, IFNγ, IL-6, and IL-17A, were increased in FcγRIIb-/- mice and etanercept antagonized these effects in FcγRIIb-/- mice. Etanercept increased serum PTH levels in the FcγRIIb-/- mouse model of lupus. Our results suggest that deletion of FcγRIIb induces osteopenia by increasing the level of proinflammatory cytokines. Etanercept is effective in preventing mandibular bone loss in FcγRIIb-/- mice, suggesting that anti-TNF-α therapy may be able to ameliorate mandibular bone loss in SLE patients with periodontitis.

摘要

系统性红斑狼疮患者由于牙周炎而导致牙槽骨丢失的风险增加，这可能是由于对口腔细菌和炎症的致病免疫反应所致。本研究旨在探讨抗 TNF-α 拮抗剂是否可以预防狼疮FcγRIIb-/- 小鼠模型下颌骨丢失。FcγRIIb 缺乏的小鼠在 6 个月时的松质骨和皮质骨体积减少。依那西普增加了 WT 和 FcγRIIb 缺陷型小鼠的松质骨体积，但不增加皮质骨体积。FcγRIIb 缺乏降低了成骨细胞标记基因 Osx、Col1a1 和 Alp 的 mRNA 水平，但对破骨细胞标记基因没有任何影响。依那西普增加了 WT 和 FcγRIIb-/- 小鼠的 Osx、Alp 和 Ocn。WT 中破骨细胞标记基因 TNF-α、Trap 和 RANKL/OPG 比值降低。FcγRIIb-/- 小鼠的促炎细胞因子 TNF-α、IFNγ、IL-6 和 IL-17A 的血清标志物增加，依那西普拮抗了 FcγRIIb-/- 小鼠的这些作用。依那西普增加了狼疮 FcγRIIb-/- 小鼠模型的血清 PTH 水平。我们的结果表明，FcγRIIb 的缺失通过增加促炎细胞因子的水平诱导骨质疏松症。依那西普可有效预防 FcγRIIb-/- 小鼠下颌骨丢失，提示抗 TNF-α 治疗可能能够改善伴牙周炎的 SLE 患者的下颌骨丢失。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7560/8051757/3d206bd52d97/pone.0250215.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7560/8051757/d4f14584cfa9/pone.0250215.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7560/8051757/c3149910b9ce/pone.0250215.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7560/8051757/b93fce44fc47/pone.0250215.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7560/8051757/3d206bd52d97/pone.0250215.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7560/8051757/d4f14584cfa9/pone.0250215.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7560/8051757/c3149910b9ce/pone.0250215.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7560/8051757/b93fce44fc47/pone.0250215.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7560/8051757/3d206bd52d97/pone.0250215.g004.jpg

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Rheumatology (Oxford). 2020 Dec 5;59(Suppl5):v4-v11. doi: 10.1093/rheumatology/keaa379.
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Host-Microbial Interactions in Systemic Lupus Erythematosus and Periodontitis.系统性红斑狼疮和牙周炎中的宿主-微生物相互作用。
Front Immunol. 2019 Nov 12;10:2602. doi: 10.3389/fimmu.2019.02602. eCollection 2019.
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Lupus-like Disease in FcγRIIB Mice Induces Osteopenia.FcγRIIB 小鼠中的狼疮样疾病导致骨质疏松症。
肿瘤坏死因子受体 1 抑制剂与牙周炎风险。
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