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ABSTRACT: Background
Individuals with chronic lung disease are at increased risk of adverse health effects from airborne particulate matter. Characterization of underlying pollutant-phenotype interactions may require comprehensive strategies. Here, a toxicogenomic approach was used to investigate how inflammation modifies the pulmonary response to urban particulate matter.Results
Transgenic mice with constitutive pulmonary overexpression of tumour necrosis factor (TNF)-alpha under the control of the surfactant protein C promoter and wildtype littermates (C57BL/6 background) were exposed by inhalation for 4 h to particulate matter (0 or 42 mg/m3 EHC-6802) and euthanized 0 or 24 h post-exposure. The low alveolar dose of particles (16 mug) did not provoke an inflammatory response in the
SUBMITTER: Thomson EM
PROVIDER: S-EPMC2661044 | biostudies-literature | 2009 Mar
REPOSITORIES: biostudies-literature