Clathrin, caveolin, or a big gulp? How tick borne pathogens enter tick cells

Clathrin, Caveolin or a Big Gulp? How tick-borne pathogens enter tick cells

Susan Noh¹, Jessica Ujczo¹, Elizabeth Hoffman², Hanen Baggar²

^1.USDA-ARS Animal Disease Research Unit, Washington State University, Pullman WA

^2.Department of Veterinary Microbiology and Pathology, Washington State University, Pullman, WA
 
            Our knowledge gaps in the understanding of tick physiology and the tick-pathogen interface impede our ability to develop better tools to prevent tick borne diseases in humans and animals.  In the case of intracellular, bacterial pathogens such as the Anaplasma spp., Ehrlichia spp, Rickettsia spp, and Francisella spp, blocking entry is a potential method for preventing transmission of tick-borne pathogens, and thus disease.  However, the molecules and mechanisms used by these pathogens to enter tick cells is unknown.   To start to fill this knowledge gap, we treated Dermacentor andersoni cells with chemicals that inhibit macropinocytosis, clathrin-dependent endocytosis, or cholesterol-dependent endocytosis, and measured the ability of A. marginale and F. novicida, both transmitted by Dermacentor andersoni ticks, to enter the treated cells.  Both A. marginale and F. novicida use clathrin-mediated endocytosis for cell entry.  F. novicida, but not A. marginale can enter tick cell using macropinocytosis.  F. novicida entry is cholesterol and caveolae-independent in D. andersoni cells, while cholesterol, but not caveolae may play a role in A. marginale entry.