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The Journal of Immunology, Vol 144, Issue 1 263-270, Copyright © 1990 by American Association of Immunologists
ARTICLES |
M Peters-Golden, RW McNish, R Hyzy, C Shelly and GB Toews
University of Michigan Medical Center, Ann Arbor 48109-0360.
The present study was undertaken to investigate the changes in arachidonic acid (AA) metabolism which accompany rat macrophage (m phi) differentiation in the lung in order to determine whether these changes occur in the alveolar space or in the pulmonary interstitium, as well as the mechanisms responsible for such changes. Metabolism of endogenous and exogenous AA by cultured m phi obtained from the peritoneum (PM), the pulmonary interstitium (IM), and the alveolar spaces (AM) was examined by using HPLC and RIA. Although PM and AM released similar amounts of endogenous AA in response to both ionophore A23187 and the particulate zymosan, PM metabolized AA predominantly to cyclooxygenase (CO) products, whereas AM produced predominantly 5- lypoxygenase (5-LO) metabolites. IM synthesized a profile of eicosanoids which more closely resembled that of PM. Studies of the metabolism of exogenously supplied AA demonstrated that AM indeed had less CO activity than did PM. PM, but not AM, CO activity decreased during prolonged culture in air, suggesting the possibility that oxidative inactivation of CO plays a role in the decline in CO capacity which accompanies m phi differentiation in the lung. In contrast, the greater expression of 5-LO metabolism in AM than PM did not reflect mere differences in enzyme capacity, since upon activation of protein kinase C with PMA or oleoylacetylglycerol, ionophore-stimulated PM produced amounts of 5-LO products which were comparable to the amounts produced by AM stimulated with A23187 alone. These results indicate that increases in 5-LO metabolism and decreases in CO metabolism accompany rat m phi differentiation in the lung, that these changes occur largely in the alveolar space, and that the increased 5-LO capacity and decreased CO capacity are independently regulated by different mechanisms.
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R. B. Covin, T. G. Brock, M. B. Bailie, and M. Peters-Golden Altered expression and localization of 5-lipoxygenase accompany macrophage differentiation in the lung Am J Physiol Lung Cell Mol Physiol, August 1, 1998; 275(2): L303 - L310. [Abstract] [Full Text] [PDF]
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P. K. Tithof, M. Peters-Golden, and P. E. Ganey Distinct Phospholipases A2 Regulate the Release of Arachidonic Acid for Eicosanoid Production and Superoxide Anion Generation in Neutrophils J. Immunol., January 15, 1998; 160(2): 953 - 960. [Abstract] [Full Text] [PDF]
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M. PETERS-GOLDEN Cell Biology of the 5-Lipoxygenase Pathway Am. J. Respir. Crit. Care Med., June 1, 1997; 157(6): 227S - 232. [Abstract] [Full Text]
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T. G. Brock, R. W. McNish, M. B. Bailie, and M. Peters-Golden Rapid Import of Cytosolic 5-Lipoxygenase into the Nucleus of Neutrophils after in Vivo Recruitment and in Vitro Adherence J. Biol. Chem., March 28, 1997; 272(13): 8276 - 8280. [Abstract] [Full Text] [PDF]
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T. G. Brock, R. W. McNish, and M. Peters-Golden Translocation and Leukotriene Synthetic Capacity of Nuclear 5-Lipoxygenase in Rat Basophilic Leukemia Cells and Alveolar Macrophages J. Biol. Chem., September 15, 1995; 270(37): 21652 - 21658. [Abstract] [Full Text] [PDF]
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T. G. Brock, E. Maydanski, R. W. McNish, and M. Peters-Golden Co-localization of Leukotriene A4 Hydrolase with 5-Lipoxygenase in Nuclei of Alveolar Macrophages and Rat Basophilic Leukemia Cells but Not Neutrophils J. Biol. Chem., September 7, 2001; 276(37): 35071 - 35077. [Abstract] [Full Text] [PDF]
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