Ticks are competent vectors for multiple pathogens that induce extreme morbidity and mortality to humans and livestock worldwide. The salivary gland is critical to the biological success of ticks indicating it may hold potential as a target tissue for acaricides. Therefore, we directly tested the hypothesis that tick salivary gland function is reliant upon epithelial transport of potassium ions and chemical modulation of inward rectifier potassium (Kir) conductance will have deleterious consequences to tick biology. Confocal fluorescent microcopy was performed to determine the spatial and temporal localization patterns of Kir channels expressed in the salivary gland. Imaging analysis indicates expression of Kir proteins in basal cells of Type III acini, which are responsible for fluid and protein secretion. Correspondingly, activation of Kir channels reduced fluid secretion from 81 ± 11 nL to less than 3 ± 1 nL with IC50 values in the low micromolar range. Interestingly, analysis of Kir protein expression in ticks that blood fed for &gt;5 days showed no expression of Kir channels, indicating Kir channels are dynamically regulated and are critical for the initial blood feeding phase but not the later. In vivo feeding assays were performed to test the hypothesis that reduced secretory activity of the salivary gland will reduce blood ingestion and that altered osmoregulation will induce mortality due to an inability to deal with the cation rich mammalian blood. Indeed, exposure to Kir channel modulators reduced the ingested volume of blood by up to 15-fold. Further, exposure to Kir channel modulators during blood feeding significantly increased the the rate of mortality with ET50 values of &lt;12 hours compared to 4.75 days for treated and control ticks, respectfully. These data strongly suggest Kir channels are critical for salivary gland function of ticks and are promising target sites for the development of novel acaricides.

Giving ticks ‘dry mouth’ through chemical modulation of inward rectifier potassium channels as a mechanism to prevent blood feeding

2019 Fall National Meeting

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