Oral Microbiology Laboratory, Institute of Microbiology Paulo de Góes, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Cellular Immunology Laboratory, Institute of Microbiology Paulo de Góes, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
J Periodontal Res. 2024 Oct;59(5):961-973. doi: 10.1111/jre.13288. Epub 2024 May 16.
Evidence suggests that translocation of oral pathogens through the oral-gut axis may induce intestinal dysbiosis. This study aimed to evaluate the impact of a highly leukotoxic Aggregatibacter actinomycetemcomitans (Aa) strain on the gut microbiota, intestinal mucosal integrity and immune system in healthy mice.
Eight-week-old male C57BL6 mice were divided into control (n = 16) and JP2 groups (n = 19), which received intragastric gavage with PBS and with a suspension of Aa JP2 (HK921), respectively, twice a week for 4 weeks. Colonic lamina propria, fecal material, serum, gingival tissues, and mandibles were obtained for analyses of leukocyte populations, inflammatory mediators, mucosal integrity, alveolar bone loss, and gut microbiota. Differences between groups for these parameters were examined by non-parametric tests.
The gut microbial richness and the number of colonic macrophages, neutrophils, and monocytes were significantly lower in Aa JP2-infected mice than in controls (p < .05). In contrast, infected animals showed higher abundance of Clostridiaceae, Lactobacillus taiwanensis, Helicobacter rodentium, higher levels of IL-6 expression in colonic tissues, and higher splenic MPO activity than controls (p < .05). No differences in tight junction expression, serum endotoxin levels, and colonic inflammatory cytokines were observed between groups. Infected animals presented also slightly more alveolar bone loss and gingival IL-6 levels than controls (p < .05).
Based on this model, intragastric administration of Aa JP2 is associated with changes in the gut ecosystem of healthy hosts, characterized by less live/recruited myeloid cells, enrichment of the gut microbiota with pathobionts and decrease in commensals. Negligible levels of colonic pro-inflammatory cytokines, and no signs of mucosal barrier disruption were related to these changes.
有证据表明，口腔病原体通过口腔-肠道轴的易位可能会诱导肠道菌群失调。本研究旨在评估高度白细胞毒性伴放线放线杆菌（Aa）菌株对健康小鼠肠道微生物群、肠道黏膜完整性和免疫系统的影响。
将 8 周龄雄性 C57BL6 小鼠分为对照组（n = 16）和 JP2 组（n = 19），分别用 PBS 和 Aa JP2（HK921）悬液进行胃内灌胃，每周两次，共 4 周。获取结肠固有层、粪便材料、血清、牙龈组织和下颌骨，用于分析白细胞群、炎症介质、黏膜完整性、牙槽骨丢失和肠道微生物群。用非参数检验比较两组间这些参数的差异。
与对照组相比，Aa JP2 感染小鼠的肠道微生物丰富度以及结肠巨噬细胞、中性粒细胞和单核细胞数量明显降低（p < .05）。相比之下，感染动物的肠道梭菌科、台湾拉氏乳杆菌、鼠型螺杆菌丰度较高，结肠组织中 IL-6 表达水平较高，脾 MPO 活性较高（p < .05）。两组间紧密连接表达、血清内毒素水平和结肠炎症细胞因子无差异。感染动物的牙槽骨丢失和牙龈 IL-6 水平也略高于对照组（p < .05）。
基于该模型，胃内给予 Aa JP2 与健康宿主肠道生态系统的变化相关，表现为活/募集的髓样细胞减少、肠道共生菌丰度增加和共生菌减少。这些变化与结肠促炎细胞因子水平低、黏膜屏障无破坏迹象有关。
