Wrann Christiane D, Winter Sebastian W, Barkhausen Tanja, Hildebrand Frank, Krettek Christian, Riedemann Niels C
Department of Trauma Surgery, Hannover Medical School, Carl Neuberg Str. 1, 30625 Hannover, Germany.
Cell Immunol. 2007 Feb;245(2):63-9. doi: 10.1016/j.cellimm.2007.04.001. Epub 2007 May 15.
C5a exerts various known harmful functions during experimental sepsis and blocking strategies demonstrated survival benefits in experimental sepsis. We investigated its potential for priming of oxidative burst in blood neutrophils and monocytes and the involvement of various signaling pathways. We here report that C5a induced priming of neutrophils and monocytes for Escherichia coli- and PMA-induced oxidative burst. This effect was strongly dependent on intact ERK1/2 signaling. P38 inhibition resulted in abrogation of C5a-induced priming only for E. coli-induced oxidative burst and PKC blockade had this effect only for PMA-induced burst. JNK inhibition had no impact. Our results demonstrate for the first time distinct involvement of ERK1/2, p38 and PKC pathways for C5a-induced priming of oxidative burst in phagocytes.
C5a在实验性脓毒症期间发挥多种已知的有害作用，阻断策略在实验性脓毒症中显示出生存益处。我们研究了其引发血液中性粒细胞和单核细胞氧化爆发的潜力以及各种信号通路的参与情况。我们在此报告，C5a诱导中性粒细胞和单核细胞对大肠杆菌和佛波酯（PMA）诱导的氧化爆发产生预激作用。这种效应强烈依赖于完整的ERK1/2信号传导。p38抑制仅导致C5a诱导的预激作用对大肠杆菌诱导的氧化爆发消失，而PKC阻断仅对PMA诱导的爆发有此作用。JNK抑制没有影响。我们的结果首次证明了ERK1/2、p38和PKC通路在C5a诱导吞噬细胞氧化爆发预激作用中的不同参与情况。
