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This Article Full Text Full Text (PDF) All Versions of this Article: 286/2/L354    most recent 00380.2002v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (8) Citing Articles via Google Scholar Google Scholar Articles by Pfau, J. C. Articles by Cramton, J. Search for Related Content PubMed PubMed Citation Articles by Pfau, J. C. Articles by Cramton, J.

Environmental oxygen tension affects phenotype in cultured bone marrow-derived macrophages

Center for Environmental Health Sciences, Department of Biomedical and Pharmaceutical Sciences, The University of Montana, Missoula, Montana 59812

Submitted 7 November 2002 ; accepted in final form 1 October 2003

This study tested the hypothesis that the unique phenotype of alveolar macrophages (AM) is maintained through adaptation to the relatively high oxygen partial pressure (Po₂) of the lung, through modification of redox-sensitive transcription factors. BALB/c mouse bone marrowderived macrophages (BMC) were differentiated under different Po₂ and compared functionally to AM and peritoneal macrophages (PM). BMC differentiated in normoxia (Po₂ 140 Torr, BMC_high) were similar to AM in having low phagocytic and antigen presenting cell (APC) activities. However, BMC grown in low oxygen tension as found in other tissues (<40 Torr, BMC_low) were better phagocytes and APCs, similar to PM. BMC_high were more oxidative intracellularly than BMC_low, based on oxidation of dichlorofluorescein and higher glutathione disulfide/glutathione (GSH) ratios, despite having more GSH. Finally, lipopolysaccharide-induced nuclear factor-B translocation, measured by laser scanning cytometry, was reduced in BMC_high and AM, compared with BMC_low and PM, respectively. These data suggest that regulation of the AM phenotype may occur, at least in part, via inhibition of NF-B by the unique redox environment.

redox; alveolar macrophage; glutathione; nuclear factor-B

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