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1 Department of Cellular and Molecular Physiology, The Pennsylvania State University College of Medicine, Hershey, PA, USA
2 Department of Pediatrics, The Pennsylvania State University College of Medicine, Hershey, PA, USA
3 Department of Cellular and Molecular Physiology, The Pennsylvania State University College of Medicine, Hershey, PA, USA; Department of Pediatrics, The Pennsylvania State University College of Medicine, Hershey, PA, USA; Department of Obstetrics and Gynecology, The Pennsylvania State University College of Medicine, Hershey, PA, USA
* To whom correspondence should be addressed. E-mail: jfloros{at}psu.edu.
Ozone (O3), a major component of air pollution and a strong oxidizing agent, can lead to lung injury associated with edema, inflammation, and epithelial cell damage. The effects of O3 on pulmonary immune cells have been studied in various in vivo and in vitro
systems. We have shown previously that O3-exposure of SP-A decreases its ability to modulate proinflammatory cytokine production by cells of monocyte/macrophage lineage (THP-1 cells). In this report, we exposed to O3, THP-1 cells and/or native SP-A obtained from bronchoalveolar lavage of patients with alveolar proteinosis, and studied cytokine production and NF-
B signaling. The results showed: 1) Exposure of THP-1 cells to O3 significantly decreased their ability to express TNF-
in response to SP-A; TNF- production, under these conditions, was still significantly higher than basal (unstimulated)
levels in filtered air (FA)-exposed THP-1 cells. 2) Exposure of both, THP-1 cells and SP-A, to O3 did not result in any significant differences in TNF- expression compared to basal levels. 3) O3 exposure of SP-A resulted in a decreased ability of SP-A to activate the NF-B pathway, as assessed by the lack of significant increase and
decrease of the nuclear p65 subunit of NF-B and cytoplasmic IB, respectively. 4) O3 exposure of THP-1 cells, resulted in a decrease in SP-A-mediated THP-1 cell responsiveness which did not seem to be mediated via the classical NF-B pathway. These findings indicate that O3 exposure may mediate its effect on macrophage function
both directly and indirectly (via SP-A oxidation) and by involving different mechanisms.
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