Ikewaki N, Tamauchi H, Inoko H
Department of Microbiology, Kitasato University School of Nursing, Japan.
Tissue Antigens. 1993 Sep;42(3):125-32. doi: 10.1111/j.1399-0039.1993.tb02178.x.
Modulation of the cellular antigens and regulation of the phagocytic activity of the monocyte-like cell line U937 after culture with lipopolysaccharide (LPS) were investigated. CD14 expression was induced on the surface of the U937 cells after 48 h of culture with LPS and then they became adhesive with numerous filamentous filopodia extruded on the cell surface, exhibiting the enhanced expression of CD16 and CD23, the activation cell surface markers for differentiation into macrophage. However, no induction or enhancement of the cell surface expression was observed with respect to CD11b, CD18, HLA-A, B, C, HLA-DR, DQ, DP or CD57. These U937 cells also acquired the ability to produce superoxide anions and to phagocytose the Salmonella enteritidis strain, 116-54. This phagocytosis was inhibited by the anti-CD11b monoclonal antibodies, but not by the anti-CD14, anti-CD16, anti-CD18, anti-CD23, anti-HLA-A, B, C or anti-HLA-DR monoclonal antibodies. These findings indicate that the phagocytic activity against Salmonella enteritidis 116-54 induced by LPS is mediated mainly via the CD11b molecule, but is not associated with the increased expression of CD11b. Puromycin and cycloheximide, inhibitors of protein synthesis, or a divalent cation-chelating agent, EDTA completely inhibited this phagocytic activity. Interestingly, EDTA was found to suppress specifically the CD11b expression on the U937 cells cultured with LPS. No phagocytic activity was induced when the U937 cells cultured with LPS were incubated at 4 degrees C, but restored to the control level when shifted up to 37 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)
研究了脂多糖(LPS)培养后单核细胞样细胞系U937的细胞抗原调节及吞噬活性。用LPS培养48小时后,U937细胞表面诱导出CD14表达,随后细胞变得具有粘附性,细胞表面伸出许多丝状伪足,CD16和CD23表达增强,这是分化为巨噬细胞的活化细胞表面标志物。然而,未观察到CD11b、CD18、HLA - A、B、C、HLA - DR、DQ、DP或CD57的细胞表面表达诱导或增强。这些U937细胞还获得了产生超氧阴离子和吞噬肠炎沙门氏菌菌株116 - 54的能力。这种吞噬作用被抗CD11b单克隆抗体抑制,但不被抗CD14、抗CD16、抗CD18、抗CD23、抗HLA - A、B、C或抗HLA - DR单克隆抗体抑制。这些发现表明,LPS诱导的对肠炎沙门氏菌116 - 54的吞噬活性主要通过CD11b分子介导,但与CD11b表达增加无关。蛋白质合成抑制剂嘌呤霉素和环己酰亚胺或二价阳离子螯合剂EDTA完全抑制了这种吞噬活性。有趣的是,发现EDTA特异性抑制用LPS培养的U937细胞上的CD11b表达。用LPS培养的U937细胞在4℃孵育时未诱导出吞噬活性,但升温至37℃时恢复到对照水平。(摘要截断于250字)