Ureaplasma parvum infection alters filamin A dynamics in host cells.
Ureaplasma parvum infection alters filamin A dynamics in host cells.
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DOI：
10.1186/1471-2334-11-101
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发表时间：
2011-04-20
影响因子：
3.7
通讯作者：
Reyes L
中科院分区：
文献类型：
--
作者：
Allam AB;Alvarez S;Brown MB;Reyes L
脲原体是从人类泌尿生殖道分离的最常见的细菌之一。脲原体可产生无症状感染或以过度炎症反应为特征的疾病。大多数研究都集中在阐明脲原体属的致病潜力，但很少注意了解这些生物体能够建立无症状感染的机制。我们采用差异蛋白质组分析的膀胱组织从大鼠实验感染U。parvum以鉴定被微生物定殖干扰的宿主细胞过程。将组织分为四类：假接种对照组、自发清除感染的动物、无症状尿路感染（UTI）和复杂性UTI。一种受感染干扰的蛋白（细丝蛋白A）被用来进一步阐明U。在人良性前列腺细胞（BPH-1）中小孢子诱导的破坏。通过共聚焦显微镜、免疫印迹和ELISA评估BPH-1细胞。膀胱组织从动物积极殖民与U。小孢子虫的肌动蛋白结合蛋白（profilin 1、黏着斑蛋白、α辅肌动蛋白和细丝蛋白A）显示出显著的改变，这些蛋白调节肌动蛋白聚合和与粘着斑形成和信号转导有关的细胞骨架功能（Fisher精确检验，P < 0.004; ANOVA，P < 0.02）。这种现象与临床特征（无症状与复杂性UTI）无关。我们选择细丝蛋白A作为进一步研究的目标。在BPH-1模型中，我们证实了U。parvum干扰细丝蛋白A的调节。具体而言，感染的BPH-1细胞表现出丝氨酸2152磷酸化的细丝蛋白A显著增加（P ≤ 0.01），这与蛋白质的蛋白水解受损及其正常的细胞内分布相关。在两种感染模型中，细丝蛋白A的动力学都受到干扰。细丝蛋白A的磷酸化响应于调节细胞运动性、分化、凋亡和炎症的各种细胞信号传导级联而发生。因此，这种现象可能是一个有用的分子标记，用于识别特定的宿主细胞途径，在U。细小病毒感染
Ureaplasmas are among the most common bacteria isolated from the human urogenital tract. Ureaplasmas can produce asymptomatic infections or disease characterized by an exaggerated inflammatory response. Most investigations have focused on elucidating the pathogenic potential of Ureaplasma species, but little attention has been paid to understanding the mechanisms by which these organisms are capable of establishing asymptomatic infection. We employed differential proteome profiling of bladder tissues from rats experimentally infected with U. parvum in order to identify host cell processes perturbed by colonization with the microbe. Tissues were grouped into four categories: sham inoculated controls, animals that spontaneously cleared infection, asymptomatic urinary tract infection (UTI), and complicated UTI. One protein that was perturbed by infection (filamin A) was used to further elucidate the mechanism of U. parvum-induced disruption in human benign prostate cells (BPH-1). BPH-1 cells were evaluated by confocal microscopy, immunoblotting and ELISA. Bladder tissue from animals actively colonized with U. parvum displayed significant alterations in actin binding proteins (profilin 1, vinculin, α actinin, and filamin A) that regulate both actin polymerization and cell cytoskeletal function pertaining to focal adhesion formation and signal transduction (Fisher's exact test, P < 0.004; ANOVA, P < 0.02). This phenomenon was independent of clinical profile (asymptomatic vs. complicated UTI). We selected filamin A as a target for additional studies. In the BPH-1 model, we confirmed that U. parvum perturbed the regulation of filamin A. Specifically, infected BPH-1 cells exhibited a significant increase in filamin A phosphorylated at serine2152 (P ≤ 0.01), which correlated with impaired proteolysis of the protein and its normal intracellular distribution. Filamin A dynamics were perturbed in both models of infection. Phosphorylation of filamin A occurs in response to various cell signaling cascades that regulate cell motility, differentiation, apoptosis and inflammation. Thus, this phenomenon may be a useful molecular marker for identifying the specific host cell pathways that are perturbed during U. parvum infection.
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影响因子：
3.7
作者：
Namiki K;Goodison S;Porvasnik S;Allan RW;Iczkowski KA;Urbanek C;Reyes L;Sakamoto N;Rosser CJ
通讯作者：
Rosser CJ
DOI：
10.1158/1078-0432.ccr-08-1402
发表时间：
2009-02-01
期刊：
Clinical cancer research : an official journal of the American Association for Cancer Research
影响因子：
--
作者：
Bedolla RG;Wang Y;Asuncion A;Chamie K;Siddiqui S;Mudryj MM;Prihoda TJ;Siddiqui J;Chinnaiyan AM;Mehra R;de Vere White RW;Ghosh PM
通讯作者：
Ghosh PM
影响因子：
4.8
作者：
Marti, A;Luo, ZJ;Avruch, J
通讯作者：
Avruch, J
影响因子：
4
作者：
Della Fazia, MA;Castelli, M;Servillo, G
通讯作者：
Servillo, G
影响因子：
6.6
作者：
Blase, Christopher;Becker, Daniel;Bereiter-Hahn, Juergen
通讯作者：
Bereiter-Hahn, Juergen