Wiener Chair and Professor, Biological Sciences

Director, LSU Superfund Research Program http://www.srp.lsu.edu/

Pennington Biomedical Research Center

6400 Perkins Road

Baton Rouge, LA  70808

Office Telephone: 225-763-2691 (PBRC)

Email: pbc@uq.edu.au

 

Projects:

Environmentally Persistent Free Radicals Alter Pulmonary Immunologic Homeostasis Resulting in Respiratory Disease 

Superfund hazardous waste sites in the US pose significant health risks to a large portion of the population, with over 22% (~73 M people) living within 4.8 km of a Superfund site. Environmental injustice is evident, as 70% of sites on the National Priorities List are located within 1.6 km of federally assisted housing. While it is recognized that living near such sites reduces life expectancy, the true extent of morbidity remains underestimated. Relationships between airborne exposures from hazardous waste remediation and respiratory diseases are not fully understood and require further research. Harmful components emitted during the thermal treatment (TT) of Superfund hazardous wastes, such as environmentally persistent free radicals (EPFRs) associated with fine and ultrafine particulate matter (PM), have been linked to respiratory concerns. We have shown that exposure of mice to aerosolized EPFRs induces a neutrophilic asthma phenotype and oxidative stress (OS) and that EPFR exposure in early childhood is associated with wheezing. We are currently exploring the role of genetic susceptibility to OS and obesity in the development and exacerbation of EPFR-induced respiratory dysfunction. The completion of these studies will provide valuable insights into risks posed by EPFRs to respiratory health and how pre-existing obesity magnifies these risks. Identifying at-risk groups for surveillance and intervention will be crucial in addressing the adverse health effects associated with hazardous waste exposure.

Elucidating Mechanisms of Mucosal Immune Protection Against Respiratory Syncytial Virus in Infants

Respiratory syncytial virus (RSV) is the number one cause of lower respiratory tract viral infection in infants and is responsible for ~60,000 in-hospital deaths annually, with most deaths occurring in infants less than three months of age. Reinfections are common, and those who develop severe bronchiolitis are at further risk of developing chronic lung diseases such as asthma. Past efforts to prevent RSV infection in infants through vaccination with formalin-inactivated virus were disastrous resulting in 80% of vaccinees being hospitalized following community-acquired RSV infection. This has hampered RSV vaccine development for nearly 50 years. Our data suggest that failure to develop protective antibody responses in the respiratory mucosa is responsible for RSV severity. We explore the validity of this hypothesis using unique sample sets from human infant RSV infection cohorts and age-relevant animal models. Data derived from these studies will have a positive paradigm-shifting impact on the understanding of severe RSV disease and yield novel immunological targets to advance pediatric vaccine design.