| First Author | Shibata Y | Year | 2006 |
| Journal | J Leukoc Biol | Volume | 80 |
| Issue | 3 | Pages | 590-8 |
| PubMed ID | 16822852 | Mgi Jnum | J:112580 |
| Mgi Id | MGI:3662801 | Doi | 10.1189/jlb.1205737 |
| Citation | Shibata Y, et al. (2006) Heat-killed BCG induces biphasic cyclooxygenase 2+ splenic macrophage formation--role of IL-10 and bone marrow precursors. J Leukoc Biol 80(3):590-8 |
| abstractText | Previous studies have shown that prostaglandin E(2) (PGE(2)) release by splenic F4/80(+) cyclooxygenase (COX)-2(+) macrophages (MO) isolated from mice, treated with mycobacterial components, plays a major role in the regulation of immune responses. However, splenic MO, isolated from untreated mice and treated in vitro with lipopolysaccharide and interferon-gamma, express COX-1 and COX-2 within 1 day but release only minimal amounts of PGE(2) following elicitation with calcium ionophore A23187. For further characterization of in vivo requirements for development of PGE(2)-releasing MO (PGE(2)-MO), C57Bl/6 [wild-type (WT)], and interleukin (IL)-10-deficient (IL-10(-/-)) mice were treated intraperitoneally with heat-killed Mycobacterium bovis bacillus Calmette-Guerin (HK-BCG). One day following injection, COX-2 was induced in splenic MO of both mouse strains. However, PGE(2) biosynthesis by these MO was not increased. Thus, expression of COX-2 is not sufficient to induce PGE(2) production in vivo or in vitro. In sharp contrast, 14 days after HK-BCG treatment, PGE(2) release by COX-2(+) splenic MO increased as much as sevenfold, and a greater increase was seen in IL-10(-/-) cells than in WT cells. To further determine whether the 14-day splenic PGE(2)-MO could be derived from bone marrow precursors, we established a chimera in which bone marrow cells were transfused from green fluorescent protein (GFP)-transgenic donors to WT mice. Donors and recipients were treated with HK-BCG simultaneously, and marrow transfusion was performed on Days 1 and 2. On Day 14 after BCG treatment, a significant number of spleen cells coexpressed COX-2 and GFP, indicating that bone marrow-derived COX-2(+) MO may be responsible for the increased PGE(2) production. |
