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Adhesin genes and proteins involved in trichomonas vaginalis cytoadherence

机译：黏附蛋白基因和蛋白质参与阴道毛滴虫的细胞粘附

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摘要

Disclosed are novel Trichomonas vaginalis adhesin cDNA and amino acid sequences, vectors and host cells. Also disclosed is an iron up- regulated promoter sequence. Methods of differential expression of a gene in the presence of iron and methods of inhibiting Trichomonas cytoadherence are also disclosed.

机译：公开了新颖的阴道毛滴虫粘附素cDNA和氨基酸序列，载体和宿主细胞。还公开了铁上调的启动子序列。还公开了在铁存在下基因的差异表达的方法和抑制滴虫的细胞粘附的方法。

著录项

公开/公告号US5922563A

专利类型
公开/公告日1999-07-13

原文格式PDF
申请/专利权人 BOARD OF REGENTS THE UNIVERSITY OF TEXAS SYSTEM;
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申请/专利号US19950504459
发明设计人 JOHN F. ALDERETE;
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申请日1995-07-20
分类号C12N15/00;
国家 US
入库时间 2022-08-22 02:07:49

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1. BACKGROUND： Vibrio vulnifi cus inside the body could activate the NF-!B signaling pathwayand initiate the inflammatory cascade. The lung is one of the earliest organs affected by sepsisassociated with acute lung injury. High mobility group protein B1 （HMGB1） is an important late-actingpro-infl ammatory cytokine involving in the pathophysiology of sepsis. It is also involved in the injuryprocess in the lung, liver and intestine. There has been no report on the involvement of HMGB1 inVibrio vulnifi cus sepsis-induced lung injury.METHODS： Sixty rats were randomly divided into a normal control group （group A, n=10） anda Vibrio vulnificus sepsis group （group B, n=50）. Sepsis was induced in the rats by subcutaneousinjection of Vibrio vulnificus （concentration 6×108 cfu/mL, volume 0.1 mL/100g）） into the left lowerlimbs. The rats in group B were sacrifi ced separately 1, 6, 12, 24, and 48 hours after the infection.Their lungs were stored as specimens, lung water content was measured, and lung pathology wasobserved under a light microscope. The expressions of the HMGB1 gene and protein in the lungswere detected by RT-PCR and Western blot. Data were analyzed with one-way analysis of variance（ANOVA） and the LSD method for pair-wise comparison between the two groups. P〈0.05 wasconsidered statistically signifi cant.RESULTS： Compared to group A （0.652±0.177）, HMGB1 mRNA expression in the lungs ofgroup B was signifi cantly higher at 0 hour （1.161±0.358, P=0.013）, 24 hours （1.679±0.235, P=0.000）,and 48 hours （1.258±0.274, P=0.004）（P〈0.05）, and peaked at 24 hours. Compared to group A（0.594±0.190）, HMGB1 protein expression at 6 hours （1.408±0.567, P=0.026） after infection wassignificantly increased （P〈0. 05）, and peaked at 24 hours （2.415±1.064, P=0.000） after infection.Compared to group A （0.699±0.054）, lung water content was significantly increased at 6 hours（0.759±0.030, P=0.001）,12 hours （0.767±0.023, P=0.000）, 24 hours （0.771±0.043, P=0.000） and 48hours （0.789±0.137, P=0.000） after infection （P〈0.05）. Compared to group A, pathological changesat 12 hours in group B indicate marked pulmonary vascular congestion, interstitial edema andinfl ammatory infi ltration. Alveolar cavity collapse and boundaries of the alveolar septum could not beclearly identifi ed.CONCLUSION： Vibrio vulnifi cus sepsis can lead to injury in rat lungs, and increased HMGB1expression in lung tissue may be one of the mechanisms for injury from Vibrio vulnifi cus sepsis. [J] . Qiao-meng Qiu ,Zhong-wang Li ,Lu-ming Tang . 世界急诊医学杂志(英文) . 2011,第4期

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3. 阴道毛滴虫黏附蛋白AP33基因的克隆及原核表达载体pET-32a（+）-ap33的构建 [A] . 毛樱逾 . 2008