Description of Research

Our overall goal is to identify mechanisms by which inhaled particles induce and/or amplify lung inflammation leading to hypersensitization and permanent lung injuries such as fibrosis. Current studies focus on the potential role(s) that defects in clearance of apoptotic cells may play in transition of particulate exposed lungs from an acute inflammatory state to a chronic disease state and the role that lung collagenases may have in hypersensitization of individuals to lung injury from particle inhalation.

Brady TC, Crapo JD, and RR Mercer. Nitric oxide inhalation transiently elevates pulmonary levels of cyclic GMP, inducible nitric oxide synthase mRNA and TNF-α. Am J Physiol, 275:L509-L515, 1998.

Aderibigbe AO, Thomas RF, Mercer RR and RL Auten. Brief exposure to 95% oxygen alters surfactant protein D and mRNA in adult rat alveolar and bronchiolar epithelium. Am J Respir Cell Mol Biol, 20:219-227, 1999.

Vlahovic G, Russell ML, Mercer RR and JD Crapo. Cellular and connective tissue changes in alveolar septal walls in emphysema. Am J Respir Crit Care Med, 160:2086- 2092, 1999.

Porter, DW, Castranova, V, Robinson, VA, Hubbs, AF, Mercer, RR, Scabilloni, J., Goldsmith, T., Schwegler-Berry, D., Battelli, L., Washko, R., Burkhart, J., Piacitelli, C., Whitmer, M. and Jones W. Acute inflammatory reaction in rat after intratracheal instillation of material collected from a nylon flocking plant. J Toxicol Environ Health 57:25-45, 1999.