One of the main goals of the Aballay lab is to understand how the nervous system regulates innate immunity. Recent studies from the lab have shown that certain neurons are specifically involved in the regulation of innate immune response in C. elegans. My secondary mentor, a post-doctoral associate in the lab, is currently studying the molecular mechanisms involved in this neural-immune communication. This is where I come in.
For the past three weeks, I have been working closely with my mentor, Genia, in determining how OCTR-1 regulates immune response. OCTR- 1 is a G-protein coupled catecholamine receptor that is expressed by sensory neurons. The Aballay lab has demonstrated that OCTR-1 functions in ASH and/or ASI sensory neurons to inhibit immune response in C. elegans. One of the main ligands that binds to this receptor is octopamine (OA), an endogenous monoamine that is structurally related to noradrenaline in vertebrates. My project involves identifying whether octopamine is crucial in influencing the OCTR-1 signals that suppress innate immunity. I am currently studying the resistance or susceptibility of three different C. elegans strains (Wildtype vs. OA deficient animals) to pathogenic infections. I have been performing killing assays, using P. aerugnosa, to assess octopamine’s influence on susceptibility to infections. At the same time, I am helping to understand the gene expression for markers of innate immune pathways in C. elegans mutants.
I am really excited about the results I have gotten so far, but I need to repeat these experiments to confirm my current data. This journey has been quite challenging, but it is also very rewarding. I am very thankful for this opportunity and for the support from my mentor and other lab personnel.