The gut microbiome shapes latitudinal differences in host immunity and pathogen load in a damselfly

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Abstract
Latitudinal patterns in fitness‐related traits within species are receiving increased attention as these inform how high‐latitude populations may evolve in response to global warming. The underlying mechanisms for these latitudinal trait patterns remain poorly understood, and recently the gut microbiome has been suggested to be a potentially important proximate driver of these patterns. We investigated the novel idea of whether the gut microbiome drives latitudinal differences in immune function and pathogen load. To test this idea, we performed a reciprocal gut microbiome transplant between slow‐paced, high‐latitude (southern Sweden) and fast‐paced, low‐latitude (southern France) populations of Ischnura elegans damselflies. The transplants were conducted in the laboratory between high‐ and low‐latitude larvae, at both a colder and warmer thermal regime, whereafter larvae were exposed to Escherichia coli, a widespread pathogenic bacterium in aquatic ecosystems. During the experiment, larval mortality, growth rate, phenoloxidase (PO) level (a measure of immune function), E. coli burden (a measure of pathogen load) and the gut microbiome diversity (α‐diversity) and community compositions (β‐diversity) were analysed. Exposure to the pathogen increased mortality, especially under warming. Our results confirmed latitude‐associated thermal adaptation and a faster pace of life of the low‐latitude larvae, which was associated with a lower immune function (lower activity of PO), consistent with previous findings and now showed this to be linked to a higher pathogen load (higher E. coli body burden). Moreover, our results provided the first experimental evidence that the gut microbiome causally contributed to latitudinal differences in the host's immune function and pathogen load. As latitudinal patterns in the microbiome are widespread, this may be an important yet ignored proximate driver of the latitudinal patterns in immune function and pathogen load.
Funding Information
  • KU Leuven (C16/17/002)
  • Fonds Wetenschappelijk Onderzoek (G.095619, G014423N)

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