Free lung cell response of mice and rats to mainstream cigarette smoke exposure |
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| Authors: | C G Gairola |
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| Affiliation: | 1. Tobacco and Health Research Institute, University of Kentucky, Lexington, Kentucky 40546-0236 USA;2. Graduate Center for Toxicology, University of Kentucky, Lexington, Kentucky 40546-0236 USA;1. Regulatory Compliance Limited, 6 Dryden Road, Loanhead, Midlothian EH20 9TY, UK;2. Centre for Inflammation Research, University of Edinburgh, Queen’s Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, UK;3. AnaPath Services GmbH, Hammerstrasse 49, 4410 Liestal, Switzerland;4. Department of Toxicology, University of Würzburg, Rhönstrasse 9, 97080 Würzburg, Germany;5. Nanoconsult, Grindakker 10, Spaubeek, The Netherlands;1. Department of Toxicology, University of Würzburg, 97078 Würzburg, Germany;2. MetaAnalyses.com, Hees, Belgium;3. Consultant Toxicology, 84503 Altötting, Germany;4. Department of Inhalation Toxicology, Fraunhofer Institute for Toxicology and Experimental Medicine ITEM, Nikolai Fuchs Strasse 1, 30625 Hannover, Germany;5. CiS Toxicology, Osorno, Chile;6. Evonik Operations GmbH, Smart Materials, Rodenbacher Chaussee 4, 63457 Hanau-Wolfgang, Germany;7. Centre for Inflammation Research, Queen''s Medical Research Institute, The University of Edinburgh, Edinburgh, UK;8. Grace Europe Holding GmbH, In der Hollerhecke 1, 67547 Worms, Germany;9. Regulatory Compliance Limited, 6 Dryden Road, Loanhead, Midlothian EH20 9TY, UK;10. Technische Universität Dresden, Institut für Verfahrenstechnik und Umwelttechnik, Dresden 01069, Germany;11. AnaPath Services GmbH, Buchsweg 4, 4625 Oberbuchsiten, Hammerstrasse 49, 4410 Liestal, Switzerland;12. MBP Holding, Heerlen, the Netherlands;13. Department of Epidemiology, Maastricht University, the Netherlands;1. Fraunhofer Institute for Toxicology and Experimental Medicine (Fraunhofer ITEM), Hannover, Germany;2. Evonik Operations GmbH, Smart Materials, Hanau, Germany;3. Grace Europe Holding GmbH, Worms, Germany;4. Institute of Process Engineering and Environmental Technology, Research Group Mechanical Process Engineering, Technische Universität Dresden (TU Dresden), Dresden, Germany;5. AnaPath Services GmbH, Liestal, Switzerland |
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| Abstract: | Male C57BL mice and F-344 rats were exposed through nose only to fresh mainstream smoke from one University of Kentucky Reference cigarette (2R1) daily under standardized conditions. At different exposure points, the lungs of room control (RM), sham control (SH), and smoke-exposed (SM) animals were lavaged and the number, composition, and properties of bronchoalveolar lavage (BAL) cells were studied. Significantly elevated levels of blood COHb and pulmonary aryl hydrocarbon hydroxylase activity indicated effective inhalation of smoke by animals. The BAL cell analysis showed that cigarette smoke induced a five- to sevenfold increase in the number of BAL cells in mice following 10- to 12-week exposure. The proportion of neutrophils (PMN) increased to about 18 +/- 3% in SM mice as compared to less than 1% in controls. Cessation of smoke treatments returned the PMN levels to those of controls within 5 weeks. Unlike mice, smoke exposure for up to 32 weeks failed to induce appreciable changes in the number and proportion of macrophages and neutrophils in rats. Large brown macrophages were observed in SM groups of both species. Functional analysis demonstrated that the BAL cells from SM mice but not rats released greater amounts of superoxides than controls under resting and phagocytically stimulated conditions. Enzymatic analysis of macrophages showed that the activity of N-acetylglucosaminidase was increased in SM groups of both species. The activity of 5'nucleotidase was significantly reduced in macrophages from SM mice but not rats. Activity of leucine aminopeptidase remained unaltered in both species. These results demonstrate distinct differences in the response of mice and rats to identically generated cigarette smoke. |
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