Schachern Patricia, Tsuprun Vladimir, Cureoglu Sebahattin, Ferrieri Patricia, Briles David, Paparella Michael, Juhn Steven
Department of Otolaryngology, University of Minnesota Medical School, Lions Research Bldg, 2001 Sixth St SE, Minneapolis, MN 55455, USA.
Arch Otolaryngol Head Neck Surg. 2008 Jun;134(6):658-62. doi: 10.1001/archotol.134.6.658.
To determine whether mutants of Streptococcus pneumoniae that are deficient in pneumococcal surface protein A (PspA), pneumococcal surface antigen A (PsaA), or pneumolysin (Ply) are less virulent and less likely to penetrate the round window membrane (RWM).
Histopathologic comparison of wild-type S. pneumoniae and its mutants deficient in PspA, PsaA, and Ply.
Otopathology Laboratory, Department of Otolaryngology, University of Minnesota Medical School, Minneapolis.
Forty young chinchillas (weight, 250-350 g) with normal external auditory canals and tympanic membranes.
Animals were divided into 3 groups and bullae inoculated with wild-type S. pneumoniae serotype 2, strain D39, or its mutants deficient in PspA, PsaA, or Ply. Two days after inoculation, bullae were processed for light microscopy and transmission electron microscopy.
Comparison of inflammatory cell infiltration and penetration of bacteria into the round window membrane and adjacent scala tympani.
Histopathologic findings using wild-type S. pneumoniae and Ply(-) mutant were similar and included otitis media and the presence of inflammatory cells and damage to and passage of bacteria through the RWM. Although otitis media was seen with the PspA(-) and PsaA(-) mutants, we observed no passage of bacteria through the RWM.
Both PspA and PsaA affect the ability of S. pneumoniae to penetrate the RWM. Understanding the role of S. pneumoniae virulence proteins in the pathogenesis of the middle ear, RWM, and inner ear will provide new strategies for the prevention and treatment of otitis media and its complications.
确定肺炎链球菌中缺乏肺炎球菌表面蛋白A(PspA)、肺炎球菌表面抗原A(PsaA)或肺炎溶血素(Ply)的突变体是否毒力较低且穿透圆窗膜(RWM)的可能性较小。
野生型肺炎链球菌及其PspA、PsaA和Ply缺陷型突变体的组织病理学比较。
明尼阿波利斯市明尼苏达大学医学院耳鼻喉科耳病理学实验室。
40只外耳道和鼓膜正常的年轻龙猫(体重250 - 350克)。
将动物分为3组,向鼓泡接种野生型2型肺炎链球菌D39株或其PspA、PsaA或Ply缺陷型突变体。接种两天后,对鼓泡进行处理以进行光学显微镜和透射电子显微镜检查。
比较炎性细胞浸润以及细菌穿透圆窗膜和邻近鼓阶的情况。
使用野生型肺炎链球菌和Ply(-)突变体的组织病理学发现相似,包括中耳炎、炎性细胞的存在以及细菌对圆窗膜的损伤和穿过情况。虽然在PspA(-)和PsaA(-)突变体中观察到中耳炎,但未观察到细菌穿过圆窗膜。
PspA和PsaA均影响肺炎链球菌穿透圆窗膜的能力。了解肺炎链球菌毒力蛋白在中耳、圆窗膜和内耳发病机制中的作用将为中耳炎及其并发症的预防和治疗提供新策略。