Oral Lactobacillus zeae exacerbates the pathological manifestation of periodontitis in a mouse model.

IF 2.8 3区 医学 Q1 DENTISTRY, ORAL SURGERY & MEDICINE
Molecular Oral Microbiology Pub Date : 2024-10-01 Epub Date: 2024-02-22 DOI:10.1111/omi.12455
Yi-Wen Chen, Yu-Wen Hou, Chuang-Wei Wang, Shih-Jung Cheng, Wei-Ting Kuo, Chun-Pin Lin, Hsin-Han Hou
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引用次数: 0

Abstract

Introduction: The worldwide prevalence of periodontitis is considerably high, and its pathogenic mechanisms must be investigated and understood in order to improve clinical treatment outcomes and reduce the disease prevalence and burden. The exacerbation of the host immune system induced by oral microbial dysbiosis and the subsequent tissue destruction are the hallmarks of the periodontitis. However, the oral bacteria involved in periodontitis are not fully understood. We used the Oxford Nanopore Technologies (ONT) sequencing system to analyze metagenomic information in subgingival dental plaque from periodontitis and non-periodontitis patients. The number of Lactobacillus zeae (L. zeae) in the periodontitis patients was 17.55-fold higher than in the non-periodontitis patients, suggesting that L. zeae is a novel periodontitis-associated pathogen. Although several Lactobacillus species are used in vivo as probiotics to treat periodontitis and compete with Porphyromonas gingivalis (P. gingivalis), the roles of L. zeae in periodontitis progression, and the relationship between L. zeae and P. gingivalis needs to be investigated.

Methods: Both L. zeae and P. gingivalis were inoculated in the ligature-implant site of periodontitis mice. We collected mouse gingival crevicular fluid to analyze inflammatory cytokine secretion using a multiplex assay. Intact or sliced mouse maxilla tissue was used for micro-computed tomography analysis or hematoxylin and eosin staining, immunohistochemistry, and tartrate-resistant acid phosphatase staining to evaluate alveolar bone loss, neutrophil infiltration, and osteoclast activation, respectively.

Results: We observed that L. zeae competed with P. gingivalis, and it increased inflammatory cytokine secretion at the ligature-implant site. Similar to P. gingivalis, L. zeae promoted ligature-induced neutrophile infiltration, osteoclast activation, and alveolar bone loss.

Discussion: We, therefore, concluded that L. zeae accelerated the progression of periodontitis in the ligature-induced periodontitis mouse model.

在小鼠模型中,口服玉米乳杆菌会加剧牙周炎的病理表现。
导言:牙周炎在全球的发病率相当高,必须研究和了解其致病机制,以改善临床治疗效果,降低疾病的发病率和负担。口腔微生物菌群失调引起的宿主免疫系统恶化和随后的组织破坏是牙周炎的特征。然而,人们对牙周炎所涉及的口腔细菌并不完全了解。我们使用牛津纳米孔技术(ONT)测序系统分析了牙周炎和非牙周炎患者龈下牙菌斑中的元基因组信息。牙周炎患者中的玉米乳杆菌(L. zeae)数量是非牙周炎患者的 17.55 倍,这表明玉米乳杆菌是一种新型的牙周炎相关病原体。尽管多种乳酸杆菌被用作治疗牙周炎的益生菌,并与牙龈卟啉单胞菌(P. gingivalis)竞争,但L. zeae在牙周炎进展中的作用以及L. zeae与P. gingivalis之间的关系仍有待研究:方法:在牙周炎小鼠的结扎-种植部位接种 L. zeae 和 P. gingivalis。我们收集了小鼠牙龈缝隙液,使用多重检测法分析炎症细胞因子的分泌情况。用完整或切片的小鼠上颌骨组织进行微型计算机断层扫描分析,或用苏木精和伊红染色、免疫组化和耐酒石酸磷酸酶染色分别评估牙槽骨损失、中性粒细胞浸润和破骨细胞活化:结果:我们观察到,L. zeae与牙龈脓毒性杆菌竞争,并增加了结扎-种植部位的炎性细胞因子分泌。与牙龈脓毒性球菌相似,L. zeae促进了结扎引起的嗜中性粒细胞浸润、破骨细胞活化和牙槽骨流失:因此,我们得出结论:在结扎诱导的牙周炎小鼠模型中,L. zeae会加速牙周炎的发展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Molecular Oral Microbiology
Molecular Oral Microbiology DENTISTRY, ORAL SURGERY & MEDICINE-MICROBIOLOGY
CiteScore
6.50
自引率
5.40%
发文量
46
审稿时长
>12 weeks
期刊介绍: Molecular Oral Microbiology publishes high quality research papers and reviews on fundamental or applied molecular studies of microorganisms of the oral cavity and respiratory tract, host-microbe interactions, cellular microbiology, molecular ecology, and immunological studies of oral and respiratory tract infections. Papers describing work in virology, or in immunology unrelated to microbial colonization or infection, will not be acceptable. Studies of the prevalence of organisms or of antimicrobials agents also are not within the scope of the journal. The journal does not publish Short Communications or Letters to the Editor. Molecular Oral Microbiology is published bimonthly.
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