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  • 1.
    Keehnen, Naomi L. P.
    et al.
    Stockholms universitet, Zoologiska institutionen.
    Kučerová, Lucie
    Stockholms universitet, Institutionen för molekylär biovetenskap, Wenner-Grens institut.
    Nylin, Sören
    Stockholms universitet, Zoologiska institutionen.
    Theopold, Ulrich
    Stockholms universitet, Institutionen för molekylär biovetenskap, Wenner-Grens institut.
    Wheat, Christopher W.
    Stockholms universitet, Zoologiska institutionen.
    Physiological Tradeoffs of Immune Response Differs by Infection Type in Pieris napi2021Inngår i: Frontiers in Physiology, E-ISSN 1664-042X, Vol. 11, artikkel-id 576797Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Understanding the tradeoffs that result from successful infection responses is central to understanding how life histories evolve. Gaining such insights, however, can be challenging, as they may be pathogen specific and confounded with experimental design. Here, we investigated whether infection from gram positive or negative bacteria results in different physiological tradeoffs, and whether these infections impact life history later in life (post-diapause development), in the butterfly Pieris napi. During the first 24 h after infection (3, 6, 12, and 24 h), after removing effects due to injection, larvae infected with Micrococcus luteus showed a strong suppression of all non-immunity related processes while several types of immune responses were upregulated. In contrast, this tradeoff between homeostasis and immune response was much less pronounced in Escherichia coli infections. These differences were also visible long after infection, via weight loss and slower development, as well as an increased mortality at higher infection levels during later stages of development. Individuals infected with M. luteus, compared to E. coli, had a higher mortality rate, and a lower pupal weight, developmental rate and adult weight. Further, males exhibited a more negative impact of infection than females. Thus, immune responses come at a cost even when the initial infection has been overcome, and these costs are likely to affect later life history parameters with fitness consequences.

  • 2.
    Keehnen, Naomi L.P.
    et al.
    Stockholms universitet, Zoologiska institutionen.
    Fors, Lisa
    Stockholms universitet, Zoologiska institutionen.
    Järver, Peter
    Stockholms universitet, Institutionen för molekylär biovetenskap, Wenner-Grens institut.
    Spetz, Anna-Lena
    Stockholms universitet, Institutionen för molekylär biovetenskap, Wenner-Grens institut.
    Nylin, Sören
    Stockholms universitet, Zoologiska institutionen.
    Theopold, Ulrich
    Stockholms universitet, Institutionen för molekylär biovetenskap, Wenner-Grens institut.
    Wheat, Christopher W.
    Stockholms universitet, Zoologiska institutionen.
    A Population Genomic Investigation of Immune Cell Diversity and Phagocytic Capacity in a Butterfly2021Inngår i: Genes, E-ISSN 2073-4425, Vol. 12, nr 2, artikkel-id 279Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Insects rely on their innate immune system to successfully mediate complex interactions with their internal microbiota, as well as the microbes present in the environment. Given the variation in microbes across habitats, the challenges to respond to them are likely to result in local adaptations in the immune system. Here we focus upon phagocytosis, a mechanism by which pathogens and foreign particles are engulfed in order to be contained, killed, and processed. We investigated the phenotypic and genetic variation related to phagocytosis in two allopatric populations of the butterfly Pieris napi. Populations were found to differ in their hemocyte composition and overall phagocytic capability, driven by the increased phagocytic propensity of each cell type. Yet, genes annotated to phagocytosis showed no large genomic signal of divergence. However, a gene set enrichment analysis on significantly divergent genes identified loci involved in glutamine metabolism, which recently have been linked to immune cell differentiation in mammals. Together these results suggest that heritable variation in phagocytic capacity arises via a quantitative trait architecture with variation in genes affecting the activation and/or differentiation of phagocytic cells, suggesting them as potential candidate genes underlying these phenotypic differences.

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