Periodontal bacteria aggravate experimental autoimmune myocarditis in mice

Periodontal bacteria aggravate experimental autoimmune myocarditis in mice
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DOI:
10.1152/ajpheart.00634.2012
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发表时间:
2013-03-01
影响因子:
4.8
通讯作者:
Isobe, Mitsuaki
Isobe, Mitsuaki
中科院分区:
医学2区
文献类型:
--
作者:
Ashigaki, Norihiko;Suzuki, Jun-ichi;Isobe, Mitsuaki

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Ashigaki N,Suzuki J,Ogawa M,Watanabe R,小林N,小林N,Hanatani T,Sekinishi A,Zempo H,Tada Y,Takamura C,和歌山K,Hirata Y,永井R,Izumi Y,Isobe M.牙周炎细菌加重小鼠实验性自身免疫性心肌炎。Am J Physiol Heart Circ Physiol 304:H740-H748,2013.首次发表于2012年12月21日; doi:10.1152/ajpheart.00634.2012.-牙周炎是人类最常见的感染之一。最近,发表的报告断言牙周炎与心血管疾病有关。虽然目前认为病毒、细菌感染和自身免疫性疾病可能是心肌炎的病因,但其发病机制尚不清楚。本研究旨在探讨牙周致病菌对实验性自身免疫性心肌炎(EAM)的影响。牙龈卟啉单胞菌(P.g.),将PBS作为对照注射到小鼠中。进行组织学和免疫组织化学分析。我们使用定量RT-PCR检测心脏mRNA水平。抗P.G.在P.g.的血浆样品中的IgG抗体水平-注射组与PBS注射组相比显著增加。组织学分析发现,P.g.-注射EAM组较PBS注射EAM组显著增加(P < 0.05)。免疫组织化学分析发现,在P.g. -注射EAM组与注射PBS EAM组比较差异有统计学意义(P < 0.05)。来自P.G.的心脏EAM组心肌组织中单核细胞趋化蛋白-1、IFN-γ和基质金属蛋白酶-9(MMP-9)mRNA的表达较EAM组显著增加(P < 0.05)。在第7天,在P.g.-注射EAM组与PBS注射EAM组比较,差异有统计学意义(P < 0.05)。这些结果表明,P.g.注射可通过CD 11b阳性细胞、细胞因子和MMP-9表达加重小鼠EAM。
Ashigaki N, Suzuki J, Ogawa M, Watanabe R, Aoyama N, Kobayashi N, Hanatani T, Sekinishi A, Zempo H, Tada Y, Takamura C, Wakayama K, Hirata Y, Nagai R, Izumi Y, Isobe M. Periodontal bacteria aggravate experimental autoimmune myocarditis in mice. Am J Physiol Heart Circ Physiol 304: H740-H748, 2013. First published December 21, 2012; doi:10.1152/ajpheart.00634.2012.-Periodontitis is one of the most common infections in humans. Recently, published reports assert that periodontitis is associated with cardiovascular disease. Although it is said that viral, bacterial infections and autoimmune diseases may be the cause of myocarditis, the pathogenesis of it remains unclear. The aim of this study was to investigate the influence of a periodontal pathogen on experimental autoimmune myocarditis (EAM). Porphyromonas gingivalis (P.g.), PBS as a control, were injected into the mice. Histopathological and immunohistochemical analyses were performed. We examined heart mRNA levels using quantitative RT-PCR. The anti-P.g. IgG antibody level in plasma samples of the P.g.-injected group significantly increased compared with the PBS-injected group. Histopathological analysis detected that the myocarditis-affected areas and the fibrotic area in the P.g.-injected EAM group significantly increased compared with the PBS-injected EAM group (P < 0.05). Immunohistochemical analysis detected that more CD11b-positive cells were shown in the heart of the P. g.-injected EAM group compared with the PBS EAM-injected group (P < 0.05). Hearts from the P. g.-injected EAM group showed significantly increased expression of monocyte chemoattractant protein-1, IFN-gamma, and matrix metalloproteinase-9 (MMP-9) mRNA compared with the hearts from the PBS-injected EAM group (P < 0.05). On day 7, serum levels of IL-6 were significantly enhanced in the P.g.-injected EAM group compared with the PBS-injected EAM group (P < 0.05). These results showed that P. g. injection could deteriorate EAM in mice through CD11b-positive cells, cytokines, and MMP-9 expression.