| First Author | Kuroda E | Year | 2003 |
| Journal | J Immunol | Volume | 170 |
| Issue | 2 | Pages | 757-64 |
| PubMed ID | 12517938 | Mgi Jnum | J:81170 |
| Mgi Id | MGI:2448200 | Doi | 10.4049/jimmunol.170.2.757 |
| Citation | Kuroda E, et al. (2003) Mechanisms of enhanced macrophage-mediated prostaglandin e(2) production and its suppressive role in Th1 activation in th2-dominant BALB/c mice. J Immunol 170(2):757-64 |
| abstractText | PGE(2) has been known to suppress Th1 responses. We studied the difference in strains of mice in PGE(2) production by macrophages and its relation to Th1 activation. Macrophages from BALB/c mice produced greater amounts of PGE(2) than those from any other strains of mice, including C57BL/6, after LPS stimulation. In accordance with the amount of PGE(2) produced, macrophage-derived IL-12 and T cell-derived IFN-gamma 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 A(2) mRNA were greater in BALB/c macrophages. However, exogenous addition of arachidonic acid did not reverse the lower production of PGE(2) by C57BL/6 macrophages. The expression of microsomal PGE synthase, a final enzyme of PGE(2) synthesis, was also greater in BALB/c macrophages. These results indicate that the greater production of PGE(2) by macrophages, which is regulated by secretory phospholipase A(2) and microsomal PGE synthase but not by cyclooxygenase-2, is related to the suppression of Th1 cytokine production in BALB/c mice. |
