Is there such a thing as a harmless parasite infection? Why does the immune system induce costs and sometimes even attack our own body, leading to devastating outcomes? Why are we ageing, and why some faster than others? These are fundamental questions in biology and medicine - and key aspects of this ERC project.
There is currently an immense interest in factors (incl. sex-specific patterns) that mediate and shape disease resistance, immune genes and immune response-related diseases (i.e. immunopathology), and how this relates to ageing and reduced lifespan. We clearly need to know more about how the immune system has evolved to optimize protection and minimize immunopathology (incl. autoimmune) costs. For this, a whole-organism approach is necessary that integrates concepts and methods of evolutionary ecology, immunology and molecular biology (a so-called ‘immunoecology approach’) – this lies at the core of my ERC AdG project ‘EcoImmuneCosts’ (EIC). This cross-disciplinary project has generated results of interest to evolutionary, behavioral and functional ecologists, but also to researchers in e.g. medicine and gerontology.
A primary target of EIC is to study the long-term consequences of low-virulent pathogens causing mild infections (previously assumed harmless), on ageing, lifetime reproductive success and lifespan - so called Darwinian fitness costs. However, the mechanisms mediating these costs are still unknown. One possible mechanism is degradation of telomeres (repetitive, non-coding DNA sequences essential for chromosome integrity and cell survival). EIC has combined correlational and experimental studies to investigate if accelerated telomere degradation can be a causative mechanism through which small immune costs (and other stressors) can accumulate and be translated into accelerated senescence and reduced Darwinian fitness. Specifically, we investigated whether there are signs of a lower ‘critical threshold’ in telomere length and patterns of TL elongation both over short and long term. Costs of infection may also be difficult to measure if there are sexually antagonistic effects on immune gene variation and regulation. The project therefore specifically targeted sex-specific immune gene variation and expression to investigate ‘hidden' immune costs of infection.
In conclusion, the EIC project has been very successful in fulfilling its project goals running large-scale long-term experiments and field studies and analysing samples. These studies have already generated exciting and novel results and I anticipate that many more will accumulate as we analyse more data.
