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15 May 2007

Volume 195, Number 10
The Journal of Infectious Diseases 2007;195:1497–1503
© 2007 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2007/19510-0015$15.00
DOI: 10.1086/514819
MAJOR ARTICLE

High‐Cholesterol Diet Facilitates Anaplasma phagocytophilum Infection and Up‐Regulates Macrophage Inflammatory Protein–2 and CXCR2 Expression in Apolipoprotein E–Deficient Mice

Qingming Xiong,

Xueqi Wang, and

Yasuko Rikihisa

Department of Veterinary Biosciences, College of Veterinary Medicine, Ohio State University, Columbus

Background.Anaplasma phagocytophilum is an obligatory intracellular bacterium that infects granulocytes and causes human granulocytic anaplasmosis (HGA). This bacterium requires cholesterol for host cell infection in vitro and incorporates exogenous cholesterol into its membrane.

Methods.To understand the role of host cholesterol in A. phagocytophilum infection in vivo, we analyzed the effects of a high‐cholesterol diet and reduced apolipoprotein E (apoE) activity on A. phagocytophilum infection in mice.

Results.A high‐cholesterol diet significantly facilitated A. phagocytophilum infection in the spleen, liver, and blood of apoE‐deficient (apoE−/−) mice, compared with the level of infection in apoE−/− mice fed a normal‐cholesterol diet or wild‐type (WT) mice fed a high‐ or normal‐cholesterol diet. A. phagocytophilum infection induced a significant elevation in the mRNA expression of macrophage inflammatory protein (MIP)–2 and an MIP‐2 receptor, CXCR2, in the spleen in apoE−/− mice fed a high‐cholesterol diet, compared with the other 3 groups.

Conclusion.Our results suggest that high blood cholesterol levels resulting from an interaction between dietary and genetic factors facilitate A. phagocytophilum infection and up‐regulate a proinflammatory chemokine and its receptor, which may contribute to HGA pathogenesis.

Received 10 August 2006; accepted 4 December 2006; electronically published 3 April 2007.

Reprints or correspondence: Dr. Yasuko Rikihisa, Dept. of Veterinary Biosciences, College of Veterinary Medicine, Ohio State University, 1925 Coffey Rd., Columbus, OH 43210‐1093 ().

Cited by

Yasuko Rikihisa, Mingqun Lin, Hua Niu, Zhihui Cheng. (2009) Type IV Secretion System of Anaplasma phagocytophilum and Ehrlichia chaffeensis. Annals of the New York Academy of Sciences 1166:1, 106-111
Online publication date: 1-Jun-2009.
CrossRef
Katharina Birkner, Birte Steiner, Christina Rinkler, Yvonne Kern, Peter Aichele, Christian Bogdan, Friederike D. von Loewenich. (2009) The elimination of Anaplasma phagocytophilum requires CD4 + T cells, but is independent of Th1 cytokines and a wide spectrum of effector mechanisms. European Journal of Immunology 38:12, 3395-3410
Online publication date: 1-Jan-2009.
CrossRef
Qingming Xiong, Weichao Bao, Yan Ge, and Yasuko Rikihisa. (2008) Ehrlichia ewingii Infection Delays Spontaneous Neutrophil Apoptosis through Stabilization of Mitochondria. The Journal of Infectious Diseases 197:8, 1110-1118
Online publication date: 15-Apr-2008.
Abstract-Full Text-PDF Version (476 kB)

  • Potential conflicts of interest: none reported.

    Financial support: National Institutes of Health (grant R01AI30010).

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