Du L, Pellen-Mussi P, Chandad F, Mouton C, Bonnaure-Mallet M
Equipe de Biologie Buccale, UPRES EA 1256, Université de Rennes I, France.
Infect Immun. 1997 Sep;65(9):3875-81. doi: 10.1128/iai.65.9.3875-3881.1997.
The mechanisms by which Porphyromonas gingivalis, a gram-negative anaerobic bacterium, is pathogenic for the periodontium remain largely hypothetical. Invasion of host tissues by P. gingivalis is believed to require adhesion of the bacterium to host cells. The aim of this study was to use monoclonal antibodies (MAbs) to characterize the bacterial cell surface component(s) acting as a ligand binding to a receptor on epithelial cells. Surface antigens of P. gingivalis ATCC 33277 were obtained as a glass bead-EDTA extract (GBE), and antiserum against the GBE was produced in rabbits. Epithelial cell membrane proteins (ECMP) were prepared from a homogenate of the SK-MES-1 cell line with Triton X-100. The antigen/ligand profile of GBE was resolved by crossed immunoaffinity electrophoresis by using ECMP in the first-dimension gel. The migration of one immunoprecipitate (IP) was retarded, indicating a ligand-receptor interaction between a surface antigen of P. gingivalis and a complementary binding site on the epithelial cell membrane. The corresponding IP in the GBE/anti-GBE immunoelectrophoresis profile was excised from replicate gels to immunize mice for production of MAbs specific for the bacterial ligand. Five MAbs were obtained and tested for reactivity with GBE in immunoblots and for inhibition of the interaction between GBE and ECMP. Immunoblots revealed polypeptides at 28, 42, 43, and 49 kDa. Inhibition tests were positive for all five MAbs. These results are conclusive evidence that the MAbs recognize functional epitopes involved in the adherence of P. gingivalis to epithelial cells and that the adhesins are likely associated with fimbriae and the hemagglutinating adhesin HA-Ag2.
牙龈卟啉单胞菌作为一种革兰氏阴性厌氧菌,其导致牙周炎的致病机制在很大程度上仍属假说。牙龈卟啉单胞菌侵袭宿主组织被认为需要该细菌黏附于宿主细胞。本研究的目的是使用单克隆抗体(MAb)来鉴定作为配体与上皮细胞受体结合的细菌细胞表面成分。牙龈卟啉单胞菌ATCC 33277的表面抗原通过玻璃珠-EDTA提取物(GBE)获得,并在兔体内产生针对GBE的抗血清。上皮细胞膜蛋白(ECMP)由SK-MES-1细胞系匀浆与Triton X-100制备而成。GBE的抗原/配体图谱通过在第一维凝胶中使用ECMP的交叉免疫亲和电泳来解析。一种免疫沉淀物(IP)的迁移受阻,表明牙龈卟啉单胞菌的表面抗原与上皮细胞膜上的互补结合位点之间存在配体-受体相互作用。从重复凝胶中切下GBE/抗GBE免疫电泳图谱中相应的IP,用于免疫小鼠以产生针对细菌配体的特异性MAb。获得了五种MAb,并在免疫印迹中测试其与GBE的反应性以及对GBE与ECMP之间相互作用的抑制作用。免疫印迹显示在28、42、43和49 kDa处有多肽。所有五种MAb的抑制试验均为阳性。这些结果是确凿的证据,表明MAb识别参与牙龈卟啉单胞菌黏附于上皮细胞的功能性表位,并且黏附素可能与菌毛和血凝黏附素HA-Ag2相关。