INTERACTION OF PNEUMOLYSIN-SUFFICIENT AND PNEUMOLYSIN-DEFICIENT ISOGENIC VARIANTS OF STREPTOCOCCUS-PNEUMONIAE WITH HUMAN RESPIRATORY MUCOSA
INTERACTION OF PNEUMOLYSIN-SUFFICIENT AND PNEUMOLYSIN-DEFICIENT ISOGENIC VARIANTS OF STREPTOCOCCUS-PNEUMONIAE WITH HUMAN RESPIRATORY MUCOSA
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DOI：
10.1128/iai.63.2.442-447.1995
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发表时间：
1995-02-01
影响因子：
3.1
通讯作者：
WILSON, R
中科院分区：
文献类型：
--
作者：
RAYNER, CFJ;JACKSON, AD;WILSON, R
肺炎链球菌是社区获得性肺炎最常见的原因，而溶血毒素肺炎毒素被认为是一个重要的毒力因素。我们研究了在空气界面的器官培养中，一株肺溶素充足的II型肺炎链球菌(PL+)和另一株相同的肺炎链球菌(PL-)与人呼吸道粘膜的相互作用。用光度技术测量纤毛搏动频率(CBF)，用扫描和透射电子显微镜评价上皮的黏附和侵袭。与对照组相比，PL+和PL-引起CBF进行性下降，其中PLC在24 h和PL-在48 h达到显著水平(P<；0.01)。培养24 h时，与对照组(P<；0.01)和PL-(P<；0.02)相比，器官培养上清液中PL+损伤的黏膜百分率显著增加。48h时，与对照组相比，PLC(P<；0.005)和PL-(P<；005)的粘膜损伤均显著增加。在24和48h，PL+和PL-主要黏附在粘液和受损细胞上，仅PL+感染引起上皮细胞间紧密连接的分离，48h时，PL+细胞黏附在其他健康的未纤毛细胞的分离边缘。P l+和P l-均引起上皮细胞超微结构损伤，肺炎链球菌感染引起呼吸道粘膜斑片状损伤，CBF降低。这些变化更严重，而且在肺炎溶血素充足的变异体中发生得更早。
Streptococcus pneumoniae is the most common cause of community-acquired pneumonia, and pneumolysin, a hemolytic toxin, is thought to be an important virulence factor. We have studied the interaction of a pneumolysin-sufficient type II S. pneumoniae strain (PL+) and an otherwise identical pneumolysin-deficient derivative (PL-) with human respiratory mucosa in an organ culture with an air interface for up to 48 h. Ciliary beat frequency (CBF) was measured by a photometric technique, and adherence to and invasion of the epithelium were assessed by scanning and transmission electron microscopy. PL+ and PL- caused a progressive fall in CBF compared with the control which became significant (P < 0.01) at 24 h for PLC and at 48 h for PL-. At 24 h, there was a significant increase in the percentage of the mucosa of the organ culture that was damaged for PL+ compared with the control (P < 0.01) and PL- (P < 0.02). At 48 h, there was a significant increase in mucosal damage for both PLC (P < 0.005) and PL- (P < 0.05) compared with the control. At 24 and 48 h, PL+ and PL- adhered predominantly to mucus and damaged cells, PL+ infection alone caused separation of tight junctions between epithelial cells, and at 48 h PL+ cells were adherent to the separated edges of otherwise healthy unciliated cells. PL+ and PL- both caused damage to the epithelial cell ultrastructure, S. pneumoniae infection caused patchy damage to the respiratory mucosa and a lowered CBF. These changes were more severe and occurred earlier with the pneumolysin-sufficient variant.