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DO ACUTE PHASE PROTEINS REFLECT SEVERITY OF INFLAMMATION IN RAT MODELS OF POLLUTANT-INDUCED LUNG INJURY?
Citation:
Schladweiler, M., D L. Andrews, P. S. Gilmour, D L. Costa, A. D. Ledbetter, AND U P. Kodavanti. DO ACUTE PHASE PROTEINS REFLECT SEVERITY OF INFLAMMATION IN RAT MODELS OF POLLUTANT-INDUCED LUNG INJURY? Presented at American Thoracic Society, Orlando, FL, May 21-26, 2004.
Description:
Title: DO ACUTE PHASE PROTEINS REFLECT THE SEVERITY OF INFLAMMATION IN RAT MODELS OF POLLUTANT-INDUCED LUNG INJURY?
M. C. Schladweiler, BS 1, P. S. Gilmour, PhD 2, D. L. Andrews, BS 1, D. L. Costa, ScD 1, A. D. Ledbetter, BS 1, K. E. Pinkerton, PhD 3 and U. P. Kodavanti, PhD 1. 1 ETD, NHEERL, US EPA, RTP, NC, United States ; 2 CEMALB, UNC, Chapel Hill, NC, United States and 3 UC Davis, Davis, CA, United States .
Increases in circulating C-reactive protein (CRP), fibrinogen, and neutrophils have been associated with air pollutant exposures in epidemiological and clinical studies. The purpose of our study was to investigate whether this systemic response can be elicited in rats exposed to a variety of pollutants, and how it may relate to the severity of lung inflammation/injury. Lung inflammation was induced in male Sprague Dawley, Wistar-Kyoto, and/or Spontaneously Hypertensive rats (60-90 d) by either intratracheal (IT) exposure to oil combustion particles (OCP; 0.0, 3.3 mg/kg) or ZnSO4 (0.0, 0.25, 0.5, 1.0 mol/kg), or by inhalation to SO2 (0, 250, 350 ppm; 5h/dx4d), concentrated ambient particles (CAPs; 0, 605-2758 g/m3; 4h/dx2d), or tobacco smoke (TS; 90 mg/m3; 6h/dx2d). BAL neutrophils, albumin, plasma fibrinogen, and rat-specific CRP were measured for up to 4 d. All exposures at the highest concentration were associated with significant inflammation following 1 d (OCP, 80%; ZnSO4, 60%; SO2, 78%, CAPs, 11-21%; ETS, 60%). The increase in fibrinogen reflected the temporal pattern of neutrophilic inflammation in the lung with all exposures. However, BAL albumin did not reflect the changes in fibrinogen as they were increased only following OCP and ZnSO4 but not following SO2, ETS, or CAPs exposures. There was a small change in CRP following each exposure relative to fibrinogen, a trend of decrease with mild neutrophilic inflammation, and a modest increase with severe neutrophilic inflammation regardless of pollutant. These data suggest that, in the rat, plasma fibrinogen is a better indicator of pulmonary inflammation than CRP. Thus, CRP measurements in rats offer limited advantage in correlating animal data with humans involving air pollution exposures. (This does not reflect US EPA policy).