Ecoimmunology
My current research explores how reproductive state affects and reproductive effort affect the strength of cellular immune responses in wolf spiders (Tigrosa georgicola).
Animals cannot maximize all their traits simultaneously. This leads to trade-offs between competing traits. Immune function is often involved in these trade-offs, because of the energetic and nutritional cost of initiating and maintaining an immune response. However, immune function not a single trait, but a collection of immune factors, that trade-off with one another as well as with non-immune traits. I seek to understand the proximate and ultimate causes of these trade-offs and investigate how they affect disease susceptibility and transmission.
Animals cannot maximize all their traits simultaneously. This leads to trade-offs between competing traits. Immune function is often involved in these trade-offs, because of the energetic and nutritional cost of initiating and maintaining an immune response. However, immune function not a single trait, but a collection of immune factors, that trade-off with one another as well as with non-immune traits. I seek to understand the proximate and ultimate causes of these trade-offs and investigate how they affect disease susceptibility and transmission.
Host-Microbiota Interactions
In my postdoctoral research and ongoing collaboration with Dr. Kat Milligan-Myhre's lab, I am investigating how neuroendocrine stress, gut microbiota, developmental stage, and host genetic background affect the inflammatory response in the gastrointestinal tract of threespine stickleback.
The microbiota that lives in a host’s gut is crucial to multiple aspects of the host’s physiology. Disturbance of normal immune responses can shift the balance between host and microbiota and result in chronic gut inflammation. Changes to the functions of the digestive and immune systems caused neuroendocrine stress have been implicated as a cause of chronic gut inflammation. However, disruptions of the microbiota can elicit similar responses and it is unclear whether IBD is regulated by top-down interactions, in which neuroendocrine stress alters microbiota via changes to gut physiology and immune responses, or by bottom-up processes, wherein changes to the microbiota alter the neuroendocrine signaling and immune response
The microbiota that lives in a host’s gut is crucial to multiple aspects of the host’s physiology. Disturbance of normal immune responses can shift the balance between host and microbiota and result in chronic gut inflammation. Changes to the functions of the digestive and immune systems caused neuroendocrine stress have been implicated as a cause of chronic gut inflammation. However, disruptions of the microbiota can elicit similar responses and it is unclear whether IBD is regulated by top-down interactions, in which neuroendocrine stress alters microbiota via changes to gut physiology and immune responses, or by bottom-up processes, wherein changes to the microbiota alter the neuroendocrine signaling and immune response
Development and Life History Trade-offs
My doctoral dissertation investigated how neuroendocrine stress can alter physiology and life history trade-offs during critical windows of development. My work in this area has focused on trade-offs between growth, development, and immune function in amphibian larvae.
For young and developing animals, such as larval amphibians, neuroendocrine stress can speed development. This allows them to escape suboptimal aquatic habitats, but can permanently alter other aspects of their phenotype, compromising fitness by reducing survival and fecundity. This outcome is primarily driven by a trade-off between developmental rate and somatic growth and has implications for immune function and nutrient homeostasis.
For young and developing animals, such as larval amphibians, neuroendocrine stress can speed development. This allows them to escape suboptimal aquatic habitats, but can permanently alter other aspects of their phenotype, compromising fitness by reducing survival and fecundity. This outcome is primarily driven by a trade-off between developmental rate and somatic growth and has implications for immune function and nutrient homeostasis.
