Viscount H B, Munro C L, Burnette-Curley D, Peterson D L, Macrina F L
Department of Microbiology and Immunology, Virginia Commonwealth University, Richmond 23298, USA.
Infect Immun. 1997 Mar;65(3):994-1002. doi: 10.1128/IAI.65.3.994-1002.1997.
FimA, a surface-associated protein of Streptococcus parasanguis, is associated with initial colonization of damaged heart tissue in an endocarditis model (D. Burnette-Curley, V. Wells, H. Viscount, C. Munro, J. Fenno, P. Fives-Taylor, and F. Macrina, Infect. Immun. 63:4669-4674, 1995). We have evaluated the efficacy of recombinant FimA as a vaccine in the rat model of endocarditis and investigated in vitro the mechanism for the protective role of immunization. FimA-immunized and nonimmunized control animals were catheterized to induce heart valve damage and infected intravenously with 10(7) CFU of wild-type S. parasanguis FW213 bacteria. The presence of bacteria associated with platelet-fibrin vegetations 24 h postchallenge was evaluated. Immunized rats were significantly less susceptible to endocarditis (2 cases among 34 animals) than the control group (21 cases among 33 animals) (P < 0.001). Incubation of S. parasanguis FW213 with rabbit anti-FimA immune serum decreased the mean percent adherence (0.34% of added cells) to platelet-fibrin matrix in vitro compared with that of preimmune normal serum (5.04% of added cells; P < 0.001). Adsorption of immune serum with FimA-positive S. parasanguis FW213 yielded antiserum that failed to block adherence to the platelet-fibrin matrix. We assessed the vaccine potential of FimA as a common immunogen able to provide cross-protection in streptococcal endocarditis by determining the occurrence and expression of fimA in the viridans group streptococci and enterococci. We detected the presence of fimA homologs by Southern hybridization and PCR amplification analyses and determined by immunoblotting the expression of FimA-like proteins among a variety of streptococci and enterococci that frequently cause endocarditis. Eighty-one percent (26 of 32) of streptococcal and enterococcal strains isolated from bacteremic patients expressed proteins that comigrated with FimA and were reactive with polyclonal anti-FimA serum. Streptococcal DNA from strains that were positive by Western blot (immunoblot) analysis hybridized to the full-length fimA probe. Our studies suggest that FimA immunization results in antibody-mediated inhibition of bacterial adherence, a critical early event in the pathogenesis of endocarditis. Our data demonstrate that a majority of streptococcal strains associated with endocarditis have genes that encode FimA-like proteins. Taken together, these results suggest that FimA is a promising candidate for an endocarditis vaccine.
血链球菌表面相关蛋白FimA与心内膜炎模型中受损心脏组织的初始定植有关(D. Burnette-Curley、V. Wells、H. Viscount、C. Munro、J. Fenno、P. Fives-Taylor和F. Macrina,《感染与免疫》63:4669 - 4674,1995年)。我们评估了重组FimA作为心内膜炎大鼠模型疫苗的效力,并在体外研究了免疫保护作用的机制。对免疫FimA和未免疫的对照动物进行插管以诱导心脏瓣膜损伤,然后静脉注射10⁷CFU野生型血链球菌FW213细菌。评估攻击后24小时与血小板 - 纤维蛋白赘生物相关的细菌的存在情况。免疫大鼠比对照组(33只动物中有21例)更不易患心内膜炎(34只动物中有2例)(P < 0.001)。与兔抗FimA免疫血清一起孵育的血链球菌FW213与预免疫正常血清相比,体外对血小板 - 纤维蛋白基质的平均黏附百分比降低(添加细胞的0.34%)(添加细胞的5.04%;P < 0.001)。用FimA阳性的血链球菌FW213吸附免疫血清产生的抗血清不能阻断对血小板 - 纤维蛋白基质的黏附。我们通过确定变形链球菌群链球菌和肠球菌中fimA的发生和表达,评估了FimA作为一种能够在链球菌性心内膜炎中提供交叉保护的常见免疫原的疫苗潜力。我们通过Southern杂交和PCR扩增分析检测fimA同源物的存在,并通过免疫印迹确定各种经常引起心内膜炎的链球菌和肠球菌中FimA样蛋白的表达。从菌血症患者中分离的81%(32株中的26株)链球菌和肠球菌菌株表达与FimA迁移一致且与多克隆抗FimA血清反应的蛋白。通过蛋白质印迹(免疫印迹)分析呈阳性的菌株的链球菌DNA与全长fimA探针杂交。我们的研究表明,FimA免疫导致抗体介导的细菌黏附抑制,这是心内膜炎发病机制中的一个关键早期事件。我们的数据表明,大多数与心内膜炎相关的链球菌菌株具有编码FimA样蛋白的基因。综上所述,这些结果表明FimA是心内膜炎疫苗的一个有前景的候选物。