Research
Innate Immune Response to Influenza Virus Infection
Influenza virus is a major health concern since it can cause severe lung infections. The innate immune system is the host’s first defense against pathogens, including influenza virus. The innate immune system consists of multiple cells including neutrophils and macrophages. Neutrophils are phagocytes that engulf and destroy pathogens through the production of reactive oxygen species (ROS). The production and release of ROS is a process called the respiratory burst response that begins with NADPH oxidase (NOX). Because ROS is highly reactive, levels must be tightly controlled to limit host tissue damage. The long-term goal of our research is to learn how to balance the respiratory burst response following IAV infection. Using a zebrafish model of influenza virus infection, our preliminary studies show that limiting ROS production improves survival. We are also investigating how low-dose arsenic exposure alters the response to influenza virus infection.
Genetic Risk Factors for Chronic Kidney Disease
Chronic Kidney Disease (CKD) is a progressive disease where kidney damage leads to defective function and can result in kidney failure. The US Centers for Disease Control and Prevention estimates that 37 million people (~15% of the US population) have CKD. In 2019, 21,820 individuals in Maine on Medicare had CKD and 1,124 of these individuals were on dialysis. Through the Maine Chronic Kidney Disease (ME-CKD) study with Northern Light Eastern Maine Medical Center Clinical Research Center, we are conducting a pilot genome-wide association study of CKD. The goals of the pilot project include 1) identify putative genetic loci that increase risk for CKD that have not been previously reported; 2) examine associations between known CKD risk loci among individuals in study; and 3) compare genetic data with other CKD studies as a way of assessing whether individuals included in the study are a representative cohort of CKD subjects.
Role of Non-Coding RNA in the Genetic Basis of Organismal Adaptation in Natural Populations
Investigate the role of non-coding RNA in the genetic basis of organismal adaptation in natural populations. A goal of my research program is to explore genetic elements and mechanisms that underlie organismal resilience and adaptive capacity. We hypothesize that genetic variation in both protein coding and non-coding genes underlie traits that confer adaptation in these natural populations. We have been studying genetic elements and mechanisms that underlie organismal resilience and adaptive capacity as part of my NSF-funded research collaboration with colleagues at University of Maine and University of New Hampshire. Our goal is to link genomic, transcriptomic and phenotypic data to organismal performance and fitness in six tidal marsh sparrow species across spatial and environmental gradients. We are working collaboratively to sequence the genomes of six sparrow species, and characterize genomic variation in populations across species, spatial and environmental gradients.
Model the Resiliency of Networks to Identify Genes that Confer Stress Resistance
Gene regulatory networks have evolved to robustly respond to perturbations that cells, tissues and organisms encounter. Our work has focused on characterizing gene regulatory networks and identifying the key regulators of those networks for tissue regeneration, an extreme example of stress resistance. We hypothesize that the resiliency of these networks must be maintained to confer stress resistance. Modeling these networks and analyzing their topology will reveal candidate genes for functionally studies.