| First Author | Kuroda E | Year | 2007 |
| Journal | Eur J Immunol | Volume | 37 |
| Issue | 8 | Pages | 2185-95 |
| PubMed ID | 17628861 | Mgi Jnum | J:123538 |
| Mgi Id | MGI:3718806 | Doi | 10.1002/eji.200737041 |
| Citation | Kuroda E, et al. (2007) IL-3 is an important differentiation factor for the development of prostaglandin E(2)-producing macrophages between C57BL/6 and BALB/c mice. Eur J Immunol 37(8):2185-95 |
| abstractText | We have previously reported that peritoneal and splenic macrophages from Th2-dominant BALB/c mice produced higher amounts of prostaglandin (PG) E(2) than cells from C57BL/6 mice. In this study, we investigated how macrophages from BALB/c mice acquire the ability of enhanced PGE(2) production, using bone marrow-derived macrophages differentiated by M-CSF, GM-CSF or IL-3. There is no strain difference in PGE(2) production by GM-CSF- and M-CSF-differentiated macrophages; however, IL-3-differentiated macrophages from BALB/c mice produced higher amounts of PGE(2) and lower amounts of type I cytokines than cells from C57BL/6 mice. IL-3-differentiated macrophages from BALB/c mice expressed larger amounts of mRNA of membrane-bound (microsomal) PGE synthase-1 (mPGES-1). The amounts of PGE(2) produced by macrophages were significantly reduced in mPGES-1-deficient mice, and these mice displayed enhanced Th1 responses after Propionibacterium acnes treatment compared with wild-type mice. Microarray analysis revealed 63 genes that are differentially expressed more than fivefold in macrophages between C57BL/6 and BALB/c mice. These results indicate that mPGES-1-mediated PGE(2) produced by macrophages regulates immune responses, and IL-3 is an important factor for the differentiation of macrophages that produce higher amounts of PGE(2) through mPGES-1 activity in BALB/c mice. |
