Oral and gum health have long been associated with incidence and outcomes of cardiovascular disease. Periodontal disease increases myocardial infarction (MI) mortality by seven-fold through mechanisms that are not fully understood. The goal of this study was to evaluate whether lipopolysaccharide (LPS) from a periodontal pathogen accelerates inflammation post-MI through memory T-cell activation. We compared 4 groups (no MI, chronic LPS, day 1 post-MI, and day 1 post-MI with chronic LPS (LPS+MI); n=68 mice) using the mouse heart attack research tool 1.0 database and tissue bank coupled with new analyses and experiments. LPS+MI increased total CD8+ T-cells in the left ventricle versus the other groups (p<0.05 versus all). Memory CD8+ T-cells (CD44+CD27+) were 10-fold greater in LPS+MI compared to MI alone (p=0.02). Interleukin (IL)-4 stimulated splenic CD8+ T-cells away from an effector phenotype and towards a memory phenotype, inducing secretion of factors associated with the Wnt/β-catenin signaling that promoted monocyte migration and decreased viability. To dissect the effect of CD8+ T-cells post-MI, we administered a major histocompatibility complex-I blocking antibody starting 7 days before MI, which prevented effector CD8+ T-cell activation without affecting the memory response. The reduction in effector cells diminished infarct wall thinning but had no effect on macrophage numbers or MertK expression. LPS+MI+IgG attenuated macrophages within the infarct without effecting CD8+ T-cells suggesting these two processes were independent. Overall, our data indicate that effector and memory CD8+ T-cells at post-MI day 1 are amplified by chronic LPS to potentially promote infarct wall thinning.

中文翻译：

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慢性牙龈卟啉单胞菌脂多糖通过激活 CD8+ T 细胞诱导不良心肌梗死伤口愈合

长期以来，口腔和牙龈健康与心血管疾病的发病率和结局相关。牙周病通过尚未完全了解的机制将心肌梗塞 (MI) 死亡率提高了七倍。本研究的目的是评估来自牙周病原体的脂多糖 (LPS) 是否通过记忆 T 细胞激活加速 MI 后的炎症。我们使用小鼠心脏病发作研究工具 1.0 数据库和耦合的组织库比较了 4 组（无 MI、慢性 LPS、MI 后第 1 天和 MI 后第 1 天与慢性 LPS (LPS+MI)；n=68 只小鼠）进行新的分析和实验。与其他组相比，LPS+MI 增加了左心室中的总 CD8+ T 细胞（与所有组相比，p<0.05）。与单独的 MI 相比，LPS+MI 中的记忆 CD8+ T 细胞 (CD44+CD27+) 高 10 倍 (p=0.02)。白细胞介素 (IL)-4 刺激脾脏 CD8+ T 细胞从效应表型转向记忆表型，诱导分泌与 Wnt/β-连环蛋白信号相关的因子，促进单核细胞迁移并降低活力。为了剖析 MI 后 CD8+ T 细胞的作用，我们在 MI 前 7 天开始施用主要组织相容性复合物-I 阻断抗体，它可以防止效应 CD8+ T 细胞活化而不影响记忆反应。效应细胞的减少减少了梗塞壁变薄，但对巨噬细胞数量或 MertK 表达没有影响。LPS+MI+IgG 在不影响 CD8+ T 细胞的情况下减弱梗塞内的巨噬细胞，表明这两个过程是独立的。全面的，