Mechanisms of Enhanced Macrophage-Mediated Prostaglandin E2 Production and Its Suppressive Role in Th1 Activation in Th2-Dominant BALB/c Mice

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  • Etsushi Kuroda
    Department of Immunology, University of Occupational and Environmental Health, School of Medicine , Kitakyushu ,
  • Uki Yamashita
    Department of Immunology, University of Occupational and Environmental Health, School of Medicine , Kitakyushu ,

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公開日
2003-01
権利情報
  • https://academic.oup.com/pages/standard-publication-reuse-rights
DOI
  • 10.4049/jimmunol.170.2.757
公開者
Oxford University Press (OUP)

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<jats:title>Abstract</jats:title> <jats:p>PGE2 has been known to suppress Th1 responses. We studied the difference in strains of mice in PGE2 production by macrophages and its relation to Th1 activation. Macrophages from BALB/c mice produced greater amounts of PGE2 than those from any other strains of mice, including C57BL/6, after LPS stimulation. In accordance with the amount of PGE2 produced, macrophage-derived IL-12 and T cell-derived IFN-γ production were more strongly suppressed in BALB/c macrophages than in C57BL/6 macrophages. When macrophages were treated with indomethacin or EP4 antagonist, Th1 cytokines were more markedly increased in cells from BALB/c mice than in those from C57BL/6 mice. Although cyclooxygenase-2 was expressed similarly after LPS stimulation in these mouse strains, the release of arachidonic acid and the expression of type V secretory phospholipase A2 mRNA were greater in BALB/c macrophages. However, exogenous addition of arachidonic acid did not reverse the lower production of PGE2 by C57BL/6 macrophages. The expression of microsomal PGE synthase, a final enzyme of PGE2 synthesis, was also greater in BALB/c macrophages. These results indicate that the greater production of PGE2 by macrophages, which is regulated by secretory phospholipase A2 and microsomal PGE synthase but not by cyclooxygenase-2, is related to the suppression of Th1 cytokine production in BALB/c mice.</jats:p>

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