Hematogenous bacterial meningitis in an intercellular adhesion molecule-1-deficient infant mouse model.
Hematogenous bacterial meningitis in an intercellular adhesion molecule-1-deficient infant mouse model.
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细胞间粘附分子 1 缺陷的婴儿小鼠模型中的血源性细菌性脑膜炎。
DOI：
10.1093/infdis/171.2.342
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Kaplan,SL
中科院分区：
文献类型：
--
作者：
Tan,TQ;Smith,CW;Hawkins,EP;MasonJr,EO;Kaplan,SL
将编码细胞间黏附分子i （ICAMI）基因基因缺陷的小鼠与野生型小鼠在注射b型流感嗜血杆菌（Hib）或肺炎链球菌后进行比较。icam - i缺陷小鼠的Hib菌血症发生率高于野生型小鼠（P= 0.007），但野生型小鼠24 h死亡率高于野生型小鼠（P= 0.03）。相比之下，icam - i缺陷小鼠的肺炎链球菌血症发生率相当，但24小时死亡率更高（P= 0.0003）。更多的icam - i缺陷小鼠的脑脊液Hib阳性（P= 0.04），而所有献祭动物的脑脊液培养均为肺炎链球菌阳性。脑脊液白细胞计数和脑膜和耳蜗的组织学在两组之间均无差异。在Hib感染早期，icam - 1缺乏可能具有保护作用，但在肺炎链球菌感染中具有不利影响。
Mice genetically deficient in the gene encoding for intercellular adhesion molecule-I (ICAMI) production were compared with wild-type mice after injection withHaemophilus injluenzaetype b (Hib) orStreptococcus pneumoniae.The incidence of Hib bacteremia was greater in the ICAM-I-deficient mice than wild-type mice(P= .007), but mortality was greater for wild-type mice at 24 h(P= .03). In contrast, the incidence of S.pneumoniaebacteremia was equivalent but mortality was greater in ICAM-I-deficient mice at 24 h(P= .0003). More ICAM-I-deficient mice had cerebrospinal fluid cultures (CSF) positive for Hib(P= .04), whereas all animals at sacrifice had CSF cultures positive for S.pneumoniae.CSF white blood cell counts and histology of the meninges and cochlea were no different between groups for either organism. ICAM-l deficiency may be protective early in Hib infection but has a detrimental effect inS.pneumoniaeinfection.