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KMID : 0613820100200060845
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Journal of Life Science
2010 Volume.20 No. 6 p.845 ~ p.852
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Role of Alveolar Macrophages in Productions of Prostaglandin D₂ and E₂ in the Inflamed Lung
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Joo Myung-Soo
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Abstract
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Our previous study showed that lungs infected by Pseudomonas, a gram-negative bacteria, produce prostaglandin D₂ (PGD₂) and prostaglandin E2 (PGE₂), the two major prostanoids generated by cyclooxygenase-2 (COX-2), and that the ratio of PGD₂ and PGE₂ can affect the outcome of the bacterial lung infection. In this study, we sought to uncover the mechanism that determines the ratio of PGD₂ and PGE₂ produced in lung inflammation. When treated with lipopolysaccharide (LPS), primary alveolar macrophages, extracted from mouse lung, more PGE₂ was produced than PGD₂, whereas MH-S, a murine alveolar macrophage cell line, produced more PGD₂ than PGE₂ in a similar experiment. Western blot analyses showed that the kinetics of COX-2 expression in both cell types is similar and epigenetic silencing of COX-2 expression did not affect expressions of lipocalin-PGD synthase (L-PGDS) and PGE synthase (mPGES-1), major enzymes synthesizing PGD₂ and PGE₂ in inflammation, respectively, indicating no effect of COX-2 on expressions of the two enzymes. Expressions of L-PGDS and mPGES-1 were also similar in both cell types, suggesting no effect of the two key enzymes in determining the ratio of PGD₂ and PGE₂ in these cells. A single intraperitoneal injection of LPS to C57BL/6 mice induced COX-2 expression and, similar to alveolar macrophages, produced more PGE₂ than PGD₂ in the lung. These results suggest that the differential expressions of PGD₂ and PGE₂ in the lung reflect those in alveolar macrophages and may not be directly determined by the enzymes responsible for PGD₂ and PGE₂ synthesis.
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KEYWORD
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Macrophages, prostaglandin D₂, prostaglandin E₂, lipopolysaccharide, cyclooxygenase-2, acute lung inflammation
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