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内毒素诱导的活尿路上皮细胞脱落是一种抗菌防御机制。

Endotoxin-induced shedding of viable uroepithelial cells is an antimicrobial defense mechanism.

作者信息

Aronson M, Medalia O, Amichay D, Nativ O

机构信息

Department of Histology and Cell Biology, Sackler School of Medicine, Ramat Aviv, Israel.

出版信息

Infect Immun. 1988 Jun;56(6):1615-7. doi: 10.1128/iai.56.6.1615-1617.1988.

Abstract

ICR mice were infected intravesically with a virulent (7343) or a nonvirulent (U+) Escherichia coli strain. The U+ strain induced considerably more shedding of uroepithelial cells than did the 7343 strain. The stimulus for this shedding was shown to be associated with lipopolysaccharide and was abrogated by pretreatment with aprotinin. Desquamation commenced within 1 h postinjection, and the cells that were shed proved to be viable. Comparison of C3H/HeJ and C3H mice revealed that only the latter responded to shedding inducers. However, C3H/HeJ mice succumbed to a systemic infection on injection of 10(6) U+ cells intravesically, whereas other mouse strains required a 100-fold dose of bacteria for this effect. Since the first stage of a bacterial infection entails adherence of the microbes to epithelial cells, inducible shedding is an antimicrobial defense mechanism.

摘要

将ICR小鼠经膀胱内接种强毒株(7343)或无毒株(U+)大肠杆菌。U+菌株诱导的尿路上皮细胞脱落明显多于7343菌株。已证明这种脱落的刺激与脂多糖有关,且用抑肽酶预处理可消除该刺激。脱屑在注射后1小时内开始,且脱落的细胞被证明是活的。对C3H/HeJ小鼠和C3H小鼠的比较显示,只有后者对脱落诱导剂有反应。然而,C3H/HeJ小鼠经膀胱内注射10(6)个U+细胞后会死于全身感染,而其他小鼠品系产生此效应则需要100倍剂量的细菌。由于细菌感染的第一阶段需要微生物粘附于上皮细胞,因此诱导性脱落是一种抗菌防御机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7880/259445/36d60f53abdb/iai00078-0218-a.jpg

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