Christophe T, Karlsson A, Rabiet M-J, Boulay F, Dahlgren C
DRCD/BBSI (UMR 5092, CEA/CNRS/UJF), Grenoble, Cedex, France.
Scand J Immunol. 2002 Nov;56(5):470-6. doi: 10.1046/j.1365-3083.2002.01149.x.
Lipoxin A4 (LXA4) has been shown to bind to the leucocyte formyl peptide receptor (FPR) homologue, FPRL1, without triggering the biological activities induced by other FPRL1 agonists. We investigated the direct effect of LXA4 as well as the effect on agonist-induced biological responses using transfected HL-60 cells expressing FPR, FPRL1 or FPRL2. LXA4 neither induced an intracellular rise in calcium in these transfectants nor affected the response induced by the peptide Trp-Lys-Tyr-Met-Val-Met (WKYMVM), an agonist that activates cells through FPRL1 and -2. Both agonists induced Erk-2 activation; however, the eicosanoid-induced activity was independent of FPRL1 and FPRL2. Moreover, LXA4 was unable to trigger neutrophil upregulation of complement receptor 3 and respiratory burst, and it had no effect on the responses induced by triggering with WKYMVM. We conclude that LXA4 is unable to affect the WKYMVM-induced signalling through FPRL1 and suggest that it acts through a receptor different from FPRL1.
脂氧素A4（LXA4）已被证明可与白细胞甲酰肽受体（FPR）同系物FPRL1结合，但不会触发其他FPRL1激动剂诱导的生物活性。我们使用表达FPR、FPRL1或FPRL2的转染HL-60细胞，研究了LXA4的直接作用以及对激动剂诱导的生物反应的影响。LXA4既不会在这些转染细胞中诱导细胞内钙升高，也不会影响由肽Trp-Lys-Tyr-Met-Val-Met（WKYMVM）诱导的反应，WKYMVM是一种通过FPRL1和-2激活细胞的激动剂。两种激动剂均诱导Erk-2激活；然而，类二十烷酸诱导的活性独立于FPRL1和FPRL2。此外，LXA4无法触发中性粒细胞补体受体3上调和呼吸爆发，并且对WKYMVM触发诱导的反应没有影响。我们得出结论，LXA4无法通过FPRL1影响WKYMVM诱导的信号传导，并表明它通过不同于FPRL1的受体起作用。
