Lindemann R A, Eilber F
Section of Oral Diagnosis, UCLA School of Dentistry 90024
Arch Oral Biol. 1989;34(6):459-63. doi: 10.1016/0003-9969(89)90125-8.
Lipopolysaccharide (LPS) from the Y4 strain of this bacterium, which is implicated in the pathogenesis of juvenile periodontitis, was incubated with human peripheral blood lymphocytes (PBL) and its action compared to that of LPS from Escherichia coli. Both LPS augmented cytotoxicity measured against natural killer (NK) cell-resistant tumour targets within 24 h of incubation. Cytotoxicity was exclusively found in NK-enriched low-density large granular lymphocyte fractions, as separated by Percoll gradient. LPS activated NK cells without stimulating high levels of proliferation. The minimum concentration of A. actinomycetemcomitans LPS required to activate NK cells was 1 microgram/ml; higher concentrations did not significantly increase this activation. LPS had no synergistic effect on the induction of PBL cytotoxicity by interleukin-2. In contrast, LPS pre-activated monocytes inhibited the induction of lymphocyte cytotoxicity by either interleukin-2 or LPS.
这种细菌的Y4菌株的脂多糖(LPS)与青少年牙周炎的发病机制有关,将其与人外周血淋巴细胞(PBL)一起孵育,并将其作用与大肠杆菌的LPS进行比较。两种LPS在孵育24小时内均增强了针对自然杀伤(NK)细胞抗性肿瘤靶标的细胞毒性。细胞毒性仅在通过Percoll梯度分离的富含NK的低密度大颗粒淋巴细胞组分中发现。LPS激活NK细胞而不刺激高水平的增殖。激活NK细胞所需的伴放线放线杆菌LPS的最低浓度为1微克/毫升;更高的浓度并没有显著增加这种激活。LPS对白介素-2诱导的PBL细胞毒性没有协同作用。相反,LPS预激活的单核细胞抑制白介素-2或LPS诱导的淋巴细胞细胞毒性。