The K1 serotype capsular polysaccharide of Porphyromonas gingivalis elicits chemokine production from murine macrophages that facilitates cell migration
The K1 serotype capsular polysaccharide of Porphyromonas gingivalis elicits chemokine production from murine macrophages that facilitates cell migration
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DOI：
10.1128/iai.00519-06
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发表时间：
2006-11-01
影响因子：
3.1
通讯作者：
Gibson, Frank C., III
中科院分区：
文献类型：
--
作者：
d'Empaire, Gabriela;Baer, Michael T.;Gibson, Frank C., III
牙龈卟啉单胞菌是与侵袭性全身性牙周病相关的主要微生物。之前的报告表明，封装的牙龈卟啉单胞菌菌株比未封装的菌株毒性更强。然而，荚膜多糖（CPS）对该生物体毒力的贡献却知之甚少。由于牙周病表现为由中性粒细胞和单核细胞组成的复杂炎症细胞病变，我们用热灭活的牙龈卟啉单胞菌W83、从牙龈卟啉单胞菌菌株W83纯化的CPS和七种已知血清型特异性牙龈卟啉单胞菌CPS培养小鼠腹膜巨噬细胞，并评估受攻击的巨噬细胞产生的上清液吸引幼稚炎症细胞的能力。我们还定义了针对牙龈卟啉单胞菌 CPS 抗原的 JE/MCP-1、KC、MIP-2 和 RANTES 产生。我们观察到，从与牙龈卟啉单胞菌 W83 和血清型 K1 CPS 一起孵育的巨噬细胞中收集的上清液刺激了体外细胞迁移室中幼稚小鼠骨髓来源的多形核白细胞的迁移。 W83 和 K1 血清型的 CPS 引发巨噬细胞强效趋化因子分泌模式，而 K2 至 K7 血清型特异的 CPS 刺激性明显较低。逆转录 PCR 和酶联免疫吸附测定显示，用纯化的牙龈卟啉单胞菌 W83 CPS 攻击的小鼠巨噬细胞表达 JE/MCP-1、KC、MIP-2 和 RANTES。趋化因子的产生似乎取决于暴露于牙龈卟啉单胞菌W83 CPS的剂量和时间。这些数据证明牙龈卟啉单胞菌血清型 K1 CPS 引发吞噬细胞产生趋化因子。此外，这些数据表明宿主对该抗原的反应可能有助于在牙龈卟啉单胞菌引起的牙周病期间观察到的炎症细胞病变的形成。
Porphyromonas gingivalis is the principal organism associated with aggressive forms of generalized periodontal disease. Previous reports have suggested that encapsulated P. gingivalis strains are more virulent than unencapsulated strains; however, the contribution of capsular polysaccharide (CPS) to the virulence of this organism is poorly understood. Since periodontal disease presents with a complex inflammatory cell lesion comprised of neutrophils and monocytes, we cultured murine peritoneal macrophages with heat-killed P. gingivalis W83, CPS purified from P. gingivalis strain W83, and the seven known serotype-specific P. gingivalis CPS and assessed the ability of supernatant fluids produced by challenged macrophages to attract naive inflammatory cells. We also defined JE/MCP-1, KC, MIP-2, and RANTES production in response to the P. gingivalis CPS antigens. We observed that supernatant fluids collected from macrophages incubated with P. gingivalis W83 and serotype K1 CPS stimulated the migration of naive murine bone marrow-derived polymorphonuclear leukocytes in an in vitro cell migration chamber. CPS from W83 and the K1 serotype elicited potent chemokine secretion patterns for macrophages, while those specific to serotypes K2 to K7 were significantly less stimulatory. Reverse transcription-PCR and enzyme-linked immunosorbent assay revealed JE/MCP-1, KC, MIP-2, and RANTES expression from murine macrophages which had been challenged with purified P. gingivalis W83 CPS. Chemokine production appeared to be dependent on both the dose of and time of exposure to P. gingivalis W83 CPS. These data demonstrate that the P. gingivalis serotype K1 CPS elicits chemokine production from phagocytic cells. Furthermore, these data suggest that the host response to this antigen may contribute to the formation of the inflammatory cell lesion observed during P. gingivalis-elicited periodontal disease.