Defining the pathogen induced regulation of sialostatins in the gulf-coast tick, Amblyomma maculatum

Tick-borne intracellular pathogens have developed mechanisms to survive in both arthropod vector and host, and differentially express certain genes depending on their environment.  The differential expressions of genes facilitate pathogen colonization in vector and transmission from vector to the host. The Gulf-Coast tick (Amblyomma maculatum) is emerging as an arthropod of increasing public health significance and competent vector of Rickettsia parkeri that causes a disease similar to Rocky Mountain spotted fever. Cysteine protease inhibitors (cystatins) form tight, equimolar, and reversible inhibitory complexes with papain-like cysteine proteases and play immune-modulatory role during tick feeding on the host.  In this study, we determine the role a tick protein superfamily cystatins in R. parkeri-infected A. maculatum tissues during blood-feeding on the host. Based on computational analysis, four putative secretory cystatin CDS sharing 44-49% amino acid identities with Ixodes scapularis cystatins were selected for blood-feeding and pathogen-induced gene expression analysis. The R. parkeri infection varied from 279.8 to 352.3 copies/µl and 42.4 to 22.6 copies/µl in 3 and 5 day blood-fed tick midgut and salivary gland tissues respectively. The transcriptional gene expression of putative secretory sialostatins will be discussed in the context of pathogen induced tick gene regulation.