| Project Detail |
For centuries, malaria has been a major global health concern, and despite intensive research efforts, malaria infection remains a key issue for many countries. Malaria parasites are also responsible for wildlife population declines and even extinction of many bird species. Despite being exposed to the same risk, there is a clear inter-individual variation in the susceptibility to malaria infection. Through MATHORMAL, I propose that such inter-individual variability in malaria susceptibility might be linked to both the prenatal programming of physiology by maternal hormonal effects and by initial differences in cellular ageing (i.e. assessed through telomere length). Higher exposure to certain maternal hormones can depress immunity, accelerate cellular ageing, and deregulate the protective microbiome of the uropygial gland linked to antimalarial defensive mechanisms. Thus, I hypothesize that increased prenatal exposure to certain maternal hormones could make the offspring more susceptible to malarial infections, potentially through its effects on telomeres and uropygial microbiome. To test this, I will first use artificially increased yolk hormone experiments (glucocorticoid, testosterone, and thyroid hormones) in a wild bird population and assess malaria infection intensity, immunity, telomere dynamics, and uropygial microbiome. Then, I will experimentally induce early-life telomere lengthening with TA-65 to assess the potential role that short telomeres play in malaria susceptibility. This project will advance our understanding of the inter-individual variation in malaria susceptibility, which will help to improve malaria prevention strategies. MATHORMAL will use an integrative approach at the crossroad of evolutionary ecology, ecophysiology, and parasitology and largely benefit from the dual knowledge transfer between myself (expertise in maternal hormonal effects and avian malaria) and my host group (expertise in maternal hormonal effects and telomere biology). |
