The determinants of measures of immune function in a wild mammal.

Animals make immune responses to protect themselves from infections. All animals have infections during their life: being infected is a normal part of life. Animals can be infected internally with viruses, bacteria, protozoa (single-celled animals) and worms and externally with ticks and mites.

Being infected causes harm to an animal because the infections damage and destroy cells and tissue. The immune responses that animals make to get rid of infections require a lot of energy. Therefore, overall, being infected is costly to an animal.
Wild animals have many other challenges in their lives, apart from infections. For example, they have to search for food, which might often not be very abundant. Further, individuals compete with each other for limited amounts of food. Animals also reproduce which is, again, costly in time and energy. Putting this all together means that wild animals live stressful lives. One important aspect of this stress is that animals may not have enough food and energy to make ideal immune responses or to fully invest in reproduction etc. Therefore, wild animals have to make difficult 'decisions' about how to use their limited resources to keep themselves alive and to pass on their genes.

Because of this, within a group of animals, individuals will vary in how good their immune responses are: some will make very strong responses, others very weak responses. We investigated this in a pilot project where we measured the immune responses of wild mice and, indeed, we found that different individuals vary a lot in the immune responses that they make. By comparing the immune responses of wild and laboratory mice we also found that the immune responses of wild mice are quite different to those of their laboratory cousins.

We now want to understand what aspects of a wild mouse's life determines whether it makes a very strong immune response or a very weak immune response. Laboratory studies of animals have identified lots of things that can affect immune response: we want to find out which of these matter, and how much, in wild mice. Some factors that affect immune function are sex (and sex hormones), genetics, season, age and body condition. For example the male hormone testosterone often suppresses immune responses; animals fed low-protein or low-calorie diets often make weaker or slower immune responses.

In our pilot project work we studied wild mice, Mus musculus. We particularly chose this species because this is also the laboratory mouse. There is a very detailed understanding of the immunology of laboratory mice and very many tools and reagents are available to measure their immune responses. This means that we could make very good measures of immune responses of wild mice, far better than we could for almost any other wild animal.

In the work that we are proposing we will undertake a large survey of wild mice in which we will measure their immune function together with many other aspects of their biology including sex, genetics, size, weight, percent body fat, leptin (the 'fat' hormone) concentration, sex hormone concentrations etc. We will then look for associations between these different factors and immune responses, which will therefore tell us what determines the immune responses of mice in the wild.

This will be the first study that will undertake a comprehensive study of immune function in wild mammals. The results will therefore, for the first time, allow us to understand the main controls of the immune responses of wild animals. This work will be relevant to understanding the immune function of other wild mammals and animals. This is important, not least, because immune function and its variation between individuals is important in affecting epidemics of infection and disease in wild populations.

Who will benefit from this research?
A range of groups will benefit from this research. This includes immunologists, infectious disease biologists, wildlife ecologists, host and pathogen population ecologists and conservation scientists. Depending on our results this work may also be of interest to animal nutritionists, endocrinologists and geneticists. These groups exist principally in academic research communities, but also in other research organisations (charities and QUANGOs) and interest groups, especially those with a focus and interest in wildlife biology, including conservation, especially with the perspective of environmental change. Our work will have this breadth of interest because the work is undertaking a whole-system approach to immune function of wild animals.

Our work will also be of interest to organisations (commercial and non-commercial) with interests in the control and/ or eradication of rodent pest populations. Examples are Rentokil Pest Control (UK) and the National Pest Technicians' Association (NPTA), both of whom Viney has contacts with.

How will they benefit from this research?
Academic interest groups (immunologists, infectious disease biologists and wildlife ecologists and biologists) will benefit from the new knowledge and understanding of immune function and its control in wild populations that this work will generate. Our work and findings are especially important because it will 'translate' results and understanding drawn from controlled laboratory based work to animals in natural environments.

Those groups with interest in the ecology and biology of wild animals and mammals especially those with interest in conservation and anthropogenic effects on animal populations (academic and non-academic) will also benefit from this research by the acquisition of new knowledge and understanding. Our work will also show that field immunology ('ecoimmunology') is possible and powerful and we envisage that our work will therefore stimulate the growth and development of this field.

Rodent pest eradication specialists may benefit from our work by being provided with new knowledge about their target species, from which they may envisage and develop new and alternative means for the control and eradication of rodent populations. Our work wil explain how the environment contributes to immune function; this will lead to the possibility of being able to predict the effect of specific environmental change on rodent populations. This could be used to control a population (or to enhance or sustain it).

What will be done to ensure that they have they opportunity to benefit from this research?
We shall present our results widely in the academic literature, taking care to publish (with cross referencing) in journals with an ecological focus and immunological focus, together with publication in widely read biology journals. In this way we shall make our work fully and widely available to all those who have the potential to benefit from our research. The number and breadth of our publications will be our first measure of our success in this respect. We shall also present our work at as broad range of scientific meetings (e.g. those with infectious disease, ecological, immunological interests) nationally and internationally, to bring our work and its findings to the attention of the users of our research. We will also aim to present the results of our work in NPTA publications.

To bring our work to wide interest groups we will use established forums, particularly the Bristol Festival of Nature which is a public-facing forum for environmental biology. Both Viney and Pocock have previously worked though this forum.