Krause P J, Maderazo E G, Bannon P, Kosciol K, Malech H M
Department of Pediatrics, Hartford Hospital, CT 06115.
J Lab Clin Med. 1988 Aug;112(2):208-15.
To determine whether neutrophil (PMN) dysfunction observed in patients with blunt trauma could be explained by alterations in PMN functional subpopulations and to further study the origins of PMN heterogeneity, we studied PMN subpopulations in 18 patients with severe blunt trauma by using a micropore filter chemotactic assay and a mouse monoclonal antibody (31D8 Mab). A major PMN subpopulation binds 31D8 Mab avidly (31D8 "bright") and depolarizes and responds chemotactically to formyl peptide (fMLP) and C5a; a minor PMN subpopulation binds 31D8 Mab weakly (31D8 "dull") and fails to depolarize and responds poorly to fMLP and C5a. Fourteen patients with trauma had marked alteration of PMN 31D8 expression compared with healthy controls 52% +/- 20% versus 92% +/- 4% bright PMNs, respectively (p less than 0.01). These patients also had significantly decreased PMN chemotaxis and increased band counts compared with controls 30 +/- 10 micron versus 53 +/- 19 micron (p less than 0.01) and 34% +/- 14% versus 6% +/- 1% (p less than 0.01), respectively. Four patients with less-severe injuries had unaltered 31D8 PMN expression and normal PMN chemotaxis. In patients whose band counts exceeded 20%, there was a strong correlation between the number of bands and the percentage of 31D8 dull PMNs. PMNs that weakly express the 31D8 antigen appear to be less mature than PMNs that strongly express the antigen regardless of cell morphology (i.e., bands, multilobed cells). The data suggest that the decreased PMN chemotaxis and increased infection rate in patients with blunt trauma is caused partly by an increase in the number of poorly functioning 31D8 dull PMNs.
为了确定钝性创伤患者中观察到的中性粒细胞（PMN）功能障碍是否可由PMN功能亚群的改变来解释，并进一步研究PMN异质性的起源，我们通过微孔滤膜趋化试验和小鼠单克隆抗体（31D8 Mab）研究了18例严重钝性创伤患者的PMN亚群。一个主要的PMN亚群能强烈结合31D8 Mab（31D8“明亮型”），去极化并对甲酰肽（fMLP）和C5a产生趋化反应；一个次要的PMN亚群与31D8 Mab结合较弱（31D8“暗淡型”），不能去极化且对fMLP和C5a反应较差。与健康对照相比，14例创伤患者的PMN 31D8表达有明显改变，分别为52%±20%与92%±4%的明亮型PMN（p<0.01）。与对照相比，这些患者的PMN趋化性也显著降低，杆状核细胞计数增加，分别为30±10微米与53±19微米（p<0.01）和34%±14%与6%±1%（p<0.01）。4例伤势较轻的患者31D8 PMN表达未改变，PMN趋化性正常。在杆状核细胞计数超过20%的患者中，杆状核细胞数量与31D8暗淡型PMN百分比之间存在很强的相关性。无论细胞形态（即杆状核细胞、多叶核细胞）如何，弱表达31D8抗原的PMN似乎比强表达该抗原的PMN成熟度更低。数据表明，钝性创伤患者PMN趋化性降低和感染率增加部分是由于功能不良的31D8暗淡型PMN数量增加所致。
