The soluble metals of the
pollutant, residual
oil fly ash (ROFA), have been shown to alter pulmonary bacterial clearance in rats. The goal of this study was to determine the potential effects on both the innate and adaptive lung immune responses after
bacterial infection in rats pre-exposed to the soluble metals in ROFA. Sprague-Dawley rats were intratracheally dosed (i.t.) at day 0 with ROFA (R-Total) (1.0 mg/100 g
body weight), the soluble fraction of ROFA (R-Soluble), the soluble sample subject to a
chelator (R-
Chelex), or
phosphate-buffered saline (Saline). On day 3, rats were administered an i.t. dose of 5 x 10(4)Listeria monocytogenes. On days 6, 8, and 10, bacterial pulmonary clearance was monitored and bronchoalveolar lavage (BAL) was performed on days 3 (pre-
infection), 6, 8, and 10. A concentrated first fraction of lavage fluid was retained for analysis of
lactate dehydrogenase and
albumin to assess
lung injury. BAL cell number, phenotype, and production of reactive
oxygen (ROS) and
nitrogen species (RNS) were assessed, and a variety of
cytokines were measured in the BAL fluid. Rats pre-treated with R-Soluble showed elevated
lung injury/cytotoxicity and increased cellular influx into the lungs. R-Soluble-treatment also altered ROS, RNS, and
cytokine levels, and caused a degree of macrophage and T cell inhibition. These effects of R-Soluble result in increased pulmonary bacterial burden after
infection. The results suggest that soluble metals in ROFA increase
lung injury and
inflammation, and alter both innate and adaptive pulmonary immune responses.