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Modulatory effects of ozone on THP-1 cells in response to SP-A stimulation

Departments of ¹Cellular and Molecular Physiology, ²Pediatrics, and ³Obstetrics and Gynecology, The Pennsylvania State University College of Medicine, Hershey, Pennsylvania

Submitted 5 April 2004 ; accepted in final form 28 September 2004

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 surfactant protein (SP)-A decreases its ability to modulate proinflammatory cytokine production by cells of monocyte/macrophage lineage (THP-1 cells). In this report, we exposed THP-1 cells and/or native SP-A obtained from bronchoalveolar lavage of patients with alveolar proteinosis to O₃ 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-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 with 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; and 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 classic 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.

inflammation; tumor necrosis factor-; nuclear factor-B; IB; surfactant protein A

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