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1 CEMALB, University of North Carolina, Chapel Hill, North Carolina, United States
2 Toxicology, University of North Carolina-Chapel Hill, Chapel Hill, North Carolina, United States
3 Pharmacology, University of North Carolina, North Carolina, United States
4 Immunotoxicology Branch/Experimental Toxicology Division, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, United States
5 Air Pollution Prevention and Control Division, National Risk Management Research Laboratory, Research Triangle Park, North Carolina, United States
6 University of North Carolina; University of North Carolina, United States
7 Center for Environmental Medicine and Lung Biology, University of North Carolina, School of Medicine, Chapel Hill, North Carolina, United States
8 Human Studies Division, EPA, Chapel Hill, North Carolina, United States
* To whom correspondence should be addressed. E-mail: samet.james{at}epa.gov.
In vivo exposure to diesel exhaust particles (DEP) elicits acute inflammatory responses in the lung characterized by inflammatory cell influx and elevated expression of mediators such as cytokines and chemokines. Signal transducers and activators of transcription (STATs) proteins are a family of cytoplasmic transcription factors that are key transducers of signaling in response to cytokine and growth factor stimulation. One member of the STAT family, Stat3, has been implicated as a regulator of inflammation, but has not been studied in regard to DEP exposure. The results of this study show that DEP induces Stat3 phosphorylation as early as 1 hr following stimulation, and that phosphorylated Stat3 translocated into the nucleus. Inhibition of epidermal growth factor receptor (EGFR) and Src activities by the inhibitors PD153035 and PP2, respectively, abolished the activation of Stat3 by DEP, suggesting that Stat3 activation by DEP requires EGFR and Src kinase activation. The present study suggests that oxidative stress induced by DEP may play a critical role in activating EGFR signaling, as evidenced by the fact that pretreatment with antioxidant prevented the activation of EGFR and Stat3. These findings demonstrate that DEP inhalation can activate pro-inflammatory Stat3 signaling in vitro.
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