Open Access
Molecular characterization of Ehrlichia interactions with tick cells and macrophages
Roman Reddy Ganta1,Lalitha Peddireddi1,Gwi-Moon Seo1,Sarah Elizabeth Dedonder1,Chuanmin Cheng1,Stephen Keith Chapes1
Department of Diagnostic Medicine/Pathobiology, College of Veterinary Medicine, Kansas State University, Manhattan, KS 66506, USA.
DOI: 10.2741/3449 Volume 14 Issue 9, pp.3259-3273
Published: 01 January 2009
(This article belongs to the Special Issue Biology of ticks)

Several tick-transmitted Anaplasmataceae family rickettsiales of the genera Ehrlichia and Anaplasma have been discovered in recent years. Some species are classified as pathogens causing emerging diseases with growing health concern for people. They include human monocytic ehrlichiosis, human granulocytic ewingii ehrlichiosis and human granulocytic anaplasmosis which are caused by Ehrlichia chaffeensis, E. ewingii and Anaplasma phagocytophilum, respectively. Despite the complex cellular environments and defense systems of arthropod and vertebrate hosts, rickettsials have evolved strategies to evade host clearance and persist in both vertebrate and tick host environments. For example, E. chaffeensis growing in vertebrate macrophages has distinct patterns of global host cell-specific protein expression and differs considerably in morphology compared with its growth in tick cells. Immunological studies suggest that host cell-specific differences in Ehrlichia gene expression aid the pathogen, extending its survival. Bacteria from tick cells persist longer when injected into mice compared with mammalian macrophage-grown bacteria, and the host response is also significantly different. This review presents the current understanding of tick-Ehrlichia interactions and implications for future.

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Roman Reddy Ganta, Lalitha Peddireddi, Gwi-Moon Seo, Sarah Elizabeth Dedonder, Chuanmin Cheng, Stephen Keith Chapes. Molecular characterization of Ehrlichia interactions with tick cells and macrophages. Frontiers in Bioscience-Landmark. 2009. 14(9); 3259-3273.