Managed honey bee colonies are experiencing unsustainable annual losses that are partly due to reduced immunocompetence, leading to acute viral outbreaks and mortality. To address the decline in honey bee colonies, we have focused on identifying novel physiological pathways that can mitigate virus-mediated mortality through increased immune function. Previous work has demonstrated that ATP-sensitive inward rectifier potassium (KATP) channels mediate the survival of individual honey bees during infection from a model virus, indicating that KATP channels may be linked to antiviral immunity. Interestingly, KATP channels are also known to regulate levels of reactive oxygen species (ROS), which are known to function as a stimulator of immune system function during virus infection. Thus, the overarching goal of this study is to validate the linkage between KATP channels, ROS, and bee survivorship during viral infection. Data show pinacidil, a KATP channel activator, is capable of significantly (P&lt;0.05) reducing antioxidant levels and increasing concentrations of lipid peroxidase enzymes after chemically-induction of ROS, suggesting KATP channels play a part in regulating ROS titers. Further, inducing ROS within individual honey bees through exposure to paraquat or pinacidil significantly reduced mortality in bees from colonies that had heavy mite infestations (&lt;8 mites/100 bees). when compared to bees from colonies that had low mite infestations (&lt;3 mites/100 bees). These data provide additional justification that ROS is an intermediate molecule for immune health and KATP channels are capable of regulating levels of ROS. While additional investigation is required to fully characterize the relationship between KATP channels, ROS, and antiviral immunity, this study has begun to fill significant gaps in knowledge pertaining to mechanisms honey bees use to regulate their antiviral immune response.

Toxicological relevance of potassium ion channels to honey bee immune health

2019 Fall National Meeting

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