Experimental data associated with the study "The Ixodes scapularis symbiont Rickettsia buchneri inhibits growth of pathogenic Rickettsiaceae in tick cells: implications for vector competence"

Abstract

These experimental data are made available as part of the study "The Ixodes scapularis symbiont Rickettsia buchneri inhibits growth of pathogenic Rickettsiaceae in tick cells: implications for vector competence" published in Frontiers in Veterinary Science. Abstract: The blacklegged tick Ixodes scapularis is a vector of pathogens of medical and veterinary importance in North America. Unlike other important human-biting Ixodes species however, this tick does not transmit pathogenic Rickettsia species, instead hosting a rickettsial endosymbiont, Rickettsia buchneri. A gene cluster encoding aminoglycoside antibiotic biosynthesis machinery has been identified in R. buchneri, which is not present in other rickettsiae, and therefore antibiotic production might represent a mechanism by which the endosymbiont is able to exclude pathogenic Rickettsia species from I. scapularis. This study identifies a second antibiotic cluster in R. buchneri with genes similar to polyketide/non-ribosomal peptide synthesis genes. Using cell culture experiments we provide evidence that infection of tick cells with R. buchneri, even at low rates, significantly reduces the ability of the pathogens Anaplasma phagocytophilum and R. parkeri to infect and replicate in cells, whereas the presence of low-pathogenic R. amblyommatis or the endosymbiotic R. peacockii in cells only partially reduced infection by R. parkeri. This research suggests a potential role of the endosymbiont in preventing other rickettsiae from colonizing I. scapularis and/or being transmitted transovarially. Whilst a link between the observed inhibition and antibiotic production is yet to be confirmed, this work contributes further to our understanding of rickettsial competition and how endosymbionts might alter vector competence by preventing colonization of the tick by pathogens.