Lindemann R A, Kjeldsen M, Cabret M
Section of Oral Biology, UCLA School of Dentistry 90024-1668, USA.
J Periodontal Res. 1995 Jul;30(4):264-71. doi: 10.1111/j.1600-0765.1995.tb02132.x.
Expression of the interleukin-2 receptor (IL-2R) on T cells is the molecular mechanism that initiates the G0 to G1 transition and is the critical first step for T cell proliferation in response to antigen. The effect of whole periodontal bacteria and lipopolysaccharides (LPS) on peripheral blood mononuclear cell (PBMC) IL-2R expression was examined in vitro. LPS induced a modest but significant increase in high affinity IL-2R alpha/beta (p55/p75 positive) expression on PBMC over untreated cells after 48 h culture. Addition of LPS to PBMC cultures depleted of monocytes had no effect on IL-2R expression compared to untreated cultures. Interleukin-1 (IL-1) caused a similar effect to LPS in 48 h PBMC cultures but IL-1 also increased high affinity IL-2R expression in cultures depleted of adherent mononuclear cells. When antibody to IL-1 was simultaneously added with LPS to PBMC cultures, the high affinity IL-2R inductive effect was reversed at 48 h, suggesting that the LPS effect on PBMC IL-2R was indirect, via monocytes. Whole pathogenic oral bacteria cultured with PBMC at high (100:1), but not low (10:1) bacteria:PBMC ratios had a similar effect to LPS, inducing high affinity IL-2R expression at 48 h. Increases in soluble IL-2R alpha were also measured in supernatants of PBMC incubated with periodontal bacteria compared to untreated controls. In this system, a critical threshold of bacteria was required to activate PBMC perhaps related to the quantity of cell-surface LPS presented to adherent mononuclear cells.
T细胞上白细胞介素-2受体(IL-2R)的表达是启动G0到G1期转变的分子机制,也是T细胞对抗原作出反应进行增殖的关键第一步。体外研究了全牙周细菌和脂多糖(LPS)对外周血单个核细胞(PBMC)IL-2R表达的影响。培养48小时后,与未处理的细胞相比,LPS诱导PBMC上高亲和力IL-2Rα/β(p55/p75阳性)表达出现适度但显著的增加。向去除单核细胞的PBMC培养物中添加LPS,与未处理的培养物相比,对IL-2R表达没有影响。白细胞介素-1(IL-1)在48小时的PBMC培养物中产生了与LPS类似的作用,但IL-1也增加了去除贴壁单核细胞的培养物中高亲和力IL-2R的表达。当将抗IL-1抗体与LPS同时添加到PBMC培养物中时,48小时时高亲和力IL-2R的诱导作用被逆转,这表明LPS对PBMC IL-2R的作用是通过单核细胞间接产生的。以高(100:1)而不是低(10:1)的细菌:PBMC比例与PBMC一起培养的全致病性口腔细菌产生了与LPS类似的作用,在48小时时诱导高亲和力IL-2R表达。与未处理的对照相比,在与牙周细菌一起孵育的PBMC上清液中也检测到可溶性IL-2Rα增加。在这个系统中,可能需要一个关键的细菌阈值来激活PBMC,这可能与呈递给贴壁单核细胞的细胞表面LPS数量有关。