Tang X M, Chegini N, Fay M F, Masterson B J
Institute for Wound Research, Department of Obstetrics and Gynecology, University of Florida, Gainesville, Florida 32610, USA.
Wound Repair Regen. 1995 Oct-Dec;3(4):518-26. doi: 10.1046/j.1524-475X.1995.30418.x.
The objective of the present study was to determine the effect of surgical glove powders Biosorb, Keoflo, and CaCO(3) and Hydrocote (a powder-free film; Biogel) on cytokine and eicosanoid production by lipopolysaccharide/phorbol 12-myristate 13-acetate activated and unactivated HL60, U937, and RPMI 1788 cells, human monocyte/macrophage, and B lymphocyte cell lines. The unactivated cell culture-conditioned media contained a low level of interleukin-1alpha and -1beta, granulocyte macrophage colony stimulating factor, and tumor necrosis factor-alpha, which significantly increased after activation (p < 0.05). Exposure of unactivated cells to glove powders or Hydrocote (100 microg/ml) had little effect. However, these compounds appeared to have multiple inhibitory and stimulatory action on the production of these cytokines and eicosanoids in lipopolysaccharide/phorbol 12-myristate 13-acetate activated cells. For instance, granulocyte macrophage colony stimulating factor production was inhibited only in U937 cells by Keoflo and CaCO(3), whereas, tumor necrosis factor-alpha production was stimulated by Biosorb and Keoflo in HL-60, and CaCO(3) was found to be predominantly inhibitory on tumor necrosis factor-alpha production by these cells (p < 0.05). Total transforming growth factor-beta(1) production was stimulated by Biosorb and Hydrocote in U937 and HL-60 cells, respectively, but inhibited by Keoflo in U937 cells. However, Biosorb and Keoflo inhibited transforming growth factor-beta(1) production in both HL-60 and RPMI 1788 cells, without any effect on active transforming growth factor-beta(1). With regard to eicosanoids, Biosorb and Keoflo stimulated prostaglandin E(2) production by RPMI 1788 cells, whereas it was inhibited by all glove powders in HL-60 cells. Thromboxane B(2) production was stimulated by Keoflo and inhibited by CaCO(3) and Hydrocote in U937 cells. Finally, Leukotriene B(4) synthesis was found to become stimulated by Keoflo, CaCO(3), and Hydrocote in both HL60 and RPMI 1788 cells (p < 0.05). These data indicate that exposure of activated, but not unactivated, macrophages and lymphocyte to surgical glove powders and Hydrocote differentially effects the release of cytokines and eicosanoids by these cells. Considering that cytokines and eicosanoids play an important role in mediating the inflammatory and immune responses of wound healing, complications arising from glove powder exposure in vivo may involve mechanisms which alter the type and level of cytokine and eicosanoid production.
本研究的目的是确定手术手套粉末Biosorb、Keoflo、碳酸钙和Hydrocote（一种无粉薄膜；Biogel）对脂多糖/佛波醇12 - 肉豆蔻酸酯13 - 乙酸酯激活和未激活的HL60、U937和RPMI 1788细胞、人单核细胞/巨噬细胞以及B淋巴细胞系中细胞因子和类花生酸产生的影响。未激活的细胞培养条件培养基中含有低水平的白细胞介素 - 1α和 - 1β、粒细胞巨噬细胞集落刺激因子以及肿瘤坏死因子 - α，激活后这些水平显著增加（p < 0.05）。未激活的细胞暴露于手套粉末或Hydrocote（100微克/毫升）几乎没有影响。然而，这些化合物似乎对脂多糖/佛波醇12 - 肉豆蔻酸酯13 - 乙酸酯激活的细胞中这些细胞因子和类花生酸的产生具有多种抑制和刺激作用。例如，Keoflo和碳酸钙仅在U937细胞中抑制粒细胞巨噬细胞集落刺激因子的产生，而在HL - 60细胞中，Biosorb和Keoflo刺激肿瘤坏死因子 - α的产生，并且发现碳酸钙对这些细胞的肿瘤坏死因子 - α产生主要起抑制作用（p < 0.05）。在U937和HL - 60细胞中，Biosorb和Hydrocote分别刺激总转化生长因子 - β(1)的产生，但Keoflo在U937细胞中抑制其产生。然而，Biosorb和Keoflo在HL - 60和RPMI 1788细胞中均抑制转化生长因子 - β(1)的产生，对活性转化生长因子 - β(1)没有任何影响。关于类花生酸，Biosorb和Keoflo刺激RPMI 1788细胞产生前列腺素E(2)，而在HL - 60细胞中所有手套粉末均抑制其产生。在U937细胞中，Keoflo刺激血栓素B(2)的产生，而碳酸钙和Hydrocote抑制其产生。最后，发现在HL60和RPMI 1788细胞中，Keoflo、碳酸钙和Hydrocote均刺激白三烯B(4)的合成（p < 0.05）。这些数据表明，激活而非未激活的巨噬细胞和淋巴细胞暴露于手术手套粉末和Hydrocote会对这些细胞中细胞因子和类花生酸的释放产生不同影响。鉴于细胞因子和类花生酸在介导伤口愈合的炎症和免疫反应中起重要作用，体内手套粉末暴露引起的并发症可能涉及改变细胞因子和类花生酸产生的类型和水平的机制。
