scispace - formally typeset
Search or ask a question

Showing papers by "Mark Trinder published in 2017"


Journal ArticleDOI
TL;DR: The results suggested that the immune deficiency (Imd) pathway is necessary for D. melanogaster survival in response to IMI toxicity and potential for probiotic lactobacilli to reduce IMI-induced susceptibility to infection.
Abstract: Pesticides are used extensively in food production to maximize crop yields. However, neonicotinoid insecticides exert unintentional toxicity to honey bees (Apis mellifera) that may partially be associated with massive population declines referred to as colony collapse disorder. We hypothesized that imidacloprid (common neonicotinoid; IMI) exposure would make Drosophila melanogaster (an insect model for the honey bee) more susceptible to bacterial pathogens, heat stress, and intestinal dysbiosis. Our results suggested that the immune deficiency (Imd) pathway is necessary for D. melanogaster survival in response to IMI toxicity. IMI exposure induced alterations in the host-microbiota as noted by increased indigenous Acetobacter and Lactobacillus spp. Furthermore, sub-lethal exposure to IMI resulted in decreased D. melanogaster survival when simultaneously exposed to bacterial infection and heat stress (37 °C). This coincided with exacerbated increases in TotA and Dpt (Imd downstream pro-survival and antimicrobial genes, respectively) expression compared to controls. Supplementation of IMI-exposed D. melanogaster with Lactobacillus plantarum ATCC 14917 mitigated survival deficits following Serratia marcescens (bacterial pathogen) septic infection. These findings support the insidious toxicity of neonicotinoid pesticides and potential for probiotic lactobacilli to reduce IMI-induced susceptibility to infection.

79 citations


Journal ArticleDOI
TL;DR: This perspective comments on the most promising areas of microbiota research that could immediately benefit from using the D. melanogaster model to identify candidate mechanisms of host–microbe symbioses relevant to pathogen exclusion, innate immunity modulation, diet, xenobiotics, and probiotic/prebiotic properties in a high throughput manner.
Abstract: We agree no model is perfect and that D. melanogaster has its limitations like any other model. We would like to stress that we are not discrediting germ-free mouse models, but that researchers could benefit from supportive in vivo evidence (rather than in vitro) of their hypotheses before embarking down this expensive avenue. The cost and time-consuming nature of germ-free mouse studies requires strong conviction of hypotheses to warrant logical further investigation. The purpose of this perspective article is to bring attention to the under-considered areas of research that D. melanogaster may be a useful model for preliminary investigations. We highlight that the inexpensive and high-throughput D. melanogaster microbiota model can enable investigators to experiment with exploratory research questions such as probiotics, prebiotics, xenobiotics, and diet-genetic interactions before verification in costlier models. D. melanogaster microbiota simplicity also enables researchers to develop predictive models of how polymicrobial interactions affect host physiology before testing in more complex hosts (a common theme in biological animal models which you have alluded to previously). Altogether, we agree that there are limitations to the D. melanogaster model. We have now explicitly pointed out the major shortcomings of this model in the Future Directions and Conclusions section and made reference to review articles addressing these limitations in more detail. We hope this will better inform readers while also abiding to the strict space limitations inherent of perspective articles.

56 citations