期刊
JOURNAL OF INFECTIOUS DISEASES
卷 185, 期 12, 页码 1745-1753出版社
OXFORD UNIV PRESS INC
DOI: 10.1086/340818
关键词
-
资金
- NCI NIH HHS [CA 21765] Funding Source: Medline
- NIAID NIH HHS [AI 01451, AI 27913] Funding Source: Medline
New Zealand White rabbits were challenged with the wild-type (wt) group B streptococci (GBS) serotype III strain (COH1) and its isogenic nonhemolytic (NH) and hyperhemolytic (HH) mutants. Mortality differed significantly between rabbits infected with the HH mutant IN40 (67%), compared with rabbits infected with the wt COH1 strain (27%) and the NH strains COH1-20 and COH1: cyl EDeltacat (13% and 0%, respectively; P<.05). Histopathologically, disseminated septic microabscesses surrounded by necrotic foci were found exclusively in the livers of HH mutant IN40-infected animals. Serum transaminase levels were 20-fold higher in the HH-infected group, compared with rabbits infected with the other strains. Positive TUNEL (in situ terminal deoxynucleotide transferase-mediated dUTP nick end labeling) staining and activation of caspase-3 in hepatocytes were more frequent in HH-infected than in wt-infected animals and absent in the NH mutant COH1-20-infected group, indicating that GBS beta-hemolysin triggers apoptotic pathways in hepatocytes. This work provides the first evidence that GBS beta-hemolysin plays a crucial role in the pathophysiology of GBS sepsis by inducing liver failure and high mortality.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据