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嗜吞噬细胞无形体共感染改变了C3H/HeN小鼠体内伯氏疏螺旋体的种群分布。

Coinfection with Anaplasma phagocytophilum alters Borrelia burgdorferi population distribution in C3H/HeN mice.

作者信息

Holden Kevin, Hodzic Emir, Feng Sunlian, Freet Kimberly J, Lefebvre Rance B, Barthold Stephen W

机构信息

Center for Comparative Medicine, University of California at Davis, One Shields Avenue, Davis, CA 95616, USA.

出版信息

Infect Immun. 2005 Jun;73(6):3440-4. doi: 10.1128/IAI.73.6.3440-3444.2005.

Abstract

Borrelia burgdorferi, the agent of Lyme disease, and Anaplasma phagocytophilum, the agent of human anaplasmosis, are both transmitted by Ixodes sp. ticks and may occasionally coinfect a host. The population distributions of tick-transmitted B. burgdorferi infection were assessed using quantitative PCR targeting the flaB gene of B. burgdorferi in the ear, heart base, quadriceps muscle, skin, and tibiotarsal joint tissue of C3H mice previously infected with A. phagocytophilum. Population distributions of Anaplasma infection were assessed by targeting the p44 gene. A. phagocytophilum in blood and serologic response to both agents were evaluated. Spirochete numbers were increased in the ears, heart base, and skin of coinfected mice, but Anaplasma numbers remained constant. Antibody response to A. phagocytophilum, but not B. burgdorferi, was decreased in coinfected mice. These results suggest that coinfection with A. phagocytophilum and B. burgdorferi modulates pathogen burden and host antibody responses. This may be explained by the ability of A. phagocytophilum to functionally impair neutrophils, important cells in the early defense against B. burgdorferi infection.

摘要

莱姆病病原体伯氏疏螺旋体(Borrelia burgdorferi)和人粒细胞无形体病病原体嗜吞噬细胞无形体(Anaplasma phagocytophilum)均由硬蜱属(Ixodes sp.)蜱传播,且偶尔会共同感染宿主。通过针对先前感染嗜吞噬细胞无形体的C3H小鼠的耳部、心脏基部、股四头肌、皮肤和胫跗关节组织中伯氏疏螺旋体flaB基因进行定量PCR,评估蜱传播的伯氏疏螺旋体感染的种群分布。通过靶向p44基因评估无形体感染的种群分布。评估血液中的嗜吞噬细胞无形体以及对这两种病原体的血清学反应。共同感染小鼠的耳部、心脏基部和皮肤中的螺旋体数量增加,但无形体数量保持不变。共同感染小鼠对嗜吞噬细胞无形体而非伯氏疏螺旋体的抗体反应降低。这些结果表明,嗜吞噬细胞无形体和伯氏疏螺旋体共同感染会调节病原体负荷和宿主抗体反应。这可能是由于嗜吞噬细胞无形体能够在功能上损害中性粒细胞,而中性粒细胞是抵御伯氏疏螺旋体感染早期的重要细胞。

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