Journal of inflammatory bowel diseases & disorders最新文献

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In Vitro Enzymatic Virulence Factors of Dermatophytes Species Isolated From Clinical Specimens 临床标本分离的皮肤真菌的体外酶毒力因子研究

Journal of inflammatory bowel diseases & disorders

Pub Date : 2022-03-01 DOI: 10.32598/jid.26.1.8

F. Mohammadi, Amirhossein Gholamlou, M. Mirzadeh, Z. Ghasemi, Hadi Aliyari

Background: Dermatophytes are keratinophilic fungi that affect the stratum corneum of the skin and keratinous structures. Violent factors play a vital role in the pathogenesis and antifungal resistance of dermatophytes. Objective: This study aims to evaluate the activity of extracellular enzymatic and biofilm formation as virulence factors of dermatophyte isolates. Methods: Fifty-eight dermatophyte isolates belonged to 27 Trichophyton. rubrum (46.6%), 19 T. mentagrophytes (32.8%), and 12 Microsporum. canis (20.7%) for evaluating the activity of phospholipase, hemolysin, proteinase, and biofilm formation were examined. The biofilm formed was analyzed by scanning electron microscopy (SEM). Findings: Evaluation of extracellular enzymes production revealed that 86.2%, 77.6 %, and 57% of dermatophyte strains were shown to be phospholipase, hemolysin, and proteinase producers, respectively. Furthermore, all isolates of T. rubrum and M. canis can produce phospholipase and hemolysin, respectively. There was a statistically significant difference between phospholipase activity and dermatophyte strains (P<0.05). In addition, biofilm formation ability was observed in 41.5% of dermatophyte isolates. The highest level of biofilm production was found in 93% of dermatophytes isolated from nail chips. A significant difference between biofilm formation with dermatophyte isolates and different body sites was observed (P <0.05). Conclusion: The activity of hydrolytic enzymes and biofilm formation as important pathogenic factors may play a role in the persistence of dermatophytosis infections. Our results showed that dermatophyte isolates have enzymatic activity and biofilm production at different levels. Therefore, understanding the function of these factors is essential to controlling the spread of dermatophytosis infection.

背景:皮肤真菌是影响皮肤角质层和角质层结构的嗜角真菌。暴力因素在皮肤真菌的发病机制和抗真菌抗性中起着至关重要的作用。目的:探讨细胞外酶活性和生物膜形成对皮肤真菌分离株的毒力影响。方法:分离的58株皮肤真菌属27种毛癣菌。红藓属植物19种(32.8%)，小孢子植物12种(46.6%)。检测了用于评价磷脂酶、溶血素、蛋白酶和生物膜形成活性的Canis(20.7%)。通过扫描电镜对所形成的生物膜进行了分析。结果:对细胞外酶产量的评估显示，86.2%、77.6%和57%的皮癣菌菌株分别产生磷脂酶、溶血素和蛋白酶。此外，所有分离株均能产生磷脂酶和溶血素。磷脂酶活性与皮癣菌间差异有统计学意义(P<0.05)。此外，41.5%的皮肤真菌分离株具有生物膜形成能力。从指甲屑中分离出的93%的皮癣菌的生物膜产量最高。分离的皮菌在不同部位的生物膜形成差异有统计学意义(P <0.05)。结论:水解酶活性和生物膜的形成可能是导致皮肤真菌感染持续存在的重要致病因素。结果表明，分离的皮癣菌具有不同水平的酶活性和生物膜产量。因此，了解这些因子的功能对控制皮肤真菌感染的传播至关重要。

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引用次数: 0

Association of Sleep Quality and Duration With Preterm Birth: The Qazvin Maternal and Neonatal Metabolic Study (QMNMS) 睡眠质量和持续时间与早产的关系:Qazvin母婴代谢研究(QMNMS)

Journal of inflammatory bowel diseases & disorders

Pub Date : 2022-03-01 DOI: 10.32598/jid.26.1.9

S. Hashemipour, F. Lalooha, Khadijeh Elmizadeh

Background: Preterm birth (PB) is a worldwide gestational problem. Poor sleep quality and short duration have been reported as possible predisposing factors of PB in some studies. Objective: This study was conducted to investigate the roles of sleep quality/duration in the occurrence of PB. Methods: This longitudinal study was performed on pregnant women with gestational age ≤14 weeks. The sleep quality was evaluated using the Pittsburgh sleep quality index (PSQI) at the first visit and women were followed until delivery. A total of 76 women with preterm and 441 women with term delivery were compared regarding the sleep quality components, sleep duration, and long or short sleep duration. The multivariate logistic regression was performed to examine the independent association of sleep quality/duration with PB. Findings: Data from 517 participants were analyzed. PB occurred in 14.7% of participants. No significant difference of 7 items of sleep quality was observed between preterm and non-preterm groups (P>0.05 for each comparison). The total PSQI score in the preterm group was significantly higher (poorer quality) compared to the non-preterm group (5.6±2.1 vs 5.3±2.4, P=0.076). In multivariate logistic regression, each unit of worsening PSQI was independently associated with a 20% higher risk of PB occurrence. Sleep duration was not associated with PB either in unadjusted or adjusted models. Conclusion: No relationship was observed between poor sleep quality (defined as PSQI>5) and PB; however, based on our results, poorer sleep quality (as a continuous variable) can be an independent risk factor for PB.

背景:早产是一个世界性的妊娠问题。一些研究报道睡眠质量差和睡眠时间短可能是诱发PB的因素。目的:探讨睡眠质量/睡眠时间在脑卒中发生中的作用。方法:对胎龄≤14周的孕妇进行纵向研究。在第一次访问时使用匹兹堡睡眠质量指数(PSQI)评估睡眠质量，并跟踪妇女直到分娩。研究人员对76名早产妇女和441名足月分娩妇女的睡眠质量、睡眠时间和睡眠时间长短进行了比较。采用多变量logistic回归检验睡眠质量/持续时间与PB的独立关联。研究结果:分析了517名参与者的数据。14.7%的参与者发生PB。早产儿组与非早产儿组7项睡眠质量比较差异均无统计学意义(P < 0.05)。早产儿组PSQI总分明显高于非早产儿组(5.6±2.1 vs 5.3±2.4,P=0.076)。在多元逻辑回归中，PSQI恶化的每个单位与PB发生风险增加20%独立相关。无论在未调整模型还是调整模型中，睡眠时间都与PB无关。结论:睡眠质量差(定义为PSQI bbb50)与PB无相关性;然而，根据我们的研究结果，较差的睡眠质量(作为一个连续变量)可能是PB的一个独立风险因素。

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引用次数: 0

Telomere Dysfunction as an Initiator of Inflammation: Clues to an Age-Old Mystery. 端粒功能障碍是炎症的发起者:一个古老谜团的线索。

Journal of inflammatory bowel diseases & disorders

Pub Date : 2021-01-01 Epub Date: 2021-02-17

Deepavali Chakravarti, Ronald A DePinho

Inflammatory Bowel Disease (IBD) is a challenging medical condition that is driven by various genetic and environmental factors. Therapeutic opportunities for this disease remain limited due to the lack of in-depth understanding of the pathogenetic mechanisms and actionable targets driving the disease. Analysis of telomere dysfunctional mice and patients with genetic defects in telomere maintenance unexpectedly revealed phenotypes mirroring those observed in IBD. Molecular characterization of this model identified a pathway driven by telomere DNA damage-mediated activation of the ATM/cABL/YAP1 pathway, which directly regulates genes central to IBD pathogenesis and amenable to therapeutic intervention. This review summarizes the evidence correlating telomere dysfunction with IBD and colitis-associated cancer and proposes therapeutic opportunities for such inflammatory conditions targeting this newly identified pathway.

炎症性肠病(IBD)是一种具有挑战性的疾病，由各种遗传和环境因素驱动。由于缺乏对该病发病机制和可操作靶点的深入了解，该病的治疗机会仍然有限。对端粒功能失调小鼠和端粒维持遗传缺陷患者的分析意外地揭示了与IBD中观察到的表型相一致的表型。该模型的分子表征确定了一条由端粒DNA损伤介导的ATM/cABL/YAP1通路激活驱动的通路，该通路直接调控IBD发病机制的核心基因，并可接受治疗干预。本综述总结了端粒功能障碍与IBD和结肠炎相关癌症相关的证据，并提出了针对这一新发现的途径治疗此类炎症的机会。

引用次数: 0

Alpha-Defensin 5 Expression is Regulated by microRNAs in the Caco-2 Intestinal Epithelial Cell Line. 在Caco-2肠上皮细胞系中α -防御素5的表达受microrna调控。

Journal of inflammatory bowel diseases & disorders

Pub Date : 2016-04-01

Donald R B Miles, Jun Shen, Alice Y Chuang, Fenshi Dong, Feng Wu, John Kwon

Background: In inflammatory bowel disease (IBD), an inappropriate immune response leads to chronic mucosal inflammation. This response may be partly due to dysregulation of defensins, which are endogenously produced antimicrobial peptides. This study determined whether microRNAs (miRNAs) regulate α-defensin 5 (DEFA5), which could further implicate both in IBD pathogenesis.

Methods: Induction of DEFA5 mRNA and protein expression was determined in Caco-2 cells. An in silico analysis identified putative miRNA binding sites of DEFA5. Expression of these miRNAs was assessed in Caco-2 cells. Regulation of DEFA5 expression by these miRNAs was measured by luciferase assays. Caco-2 cells were transfected with miR-124 and miR-924 mimics, and DEFA5 mRNA and protein expression was measured.

Results: DEFA5 mRNA and protein expression was inducible in Caco-2 cells. Fifteen putative miRNA binding sites were found in DEFA5. The expression of miR-124 and miR-924 decreased following induction. Transfection of a luciferase construct containing the DEFA5 miRNA binding sites resulted in a decrease in luciferase activity compared to transfection of the empty vector. Transfection of a reporter construct containing mismatched miRNA binding sites resulted in restoration of luciferase activities. Transfection of miRNA mimics decreased DEFA5 mRNA expression and protein expression.

Conclusions: miR-124 and miR-924 negatively regulate DEFA5 mRNA and protein expression. These data implicate miRNAs in intestinal innate immune regulation and IBD pathogenesis.

背景:在炎症性肠病(IBD)中，不适当的免疫反应导致慢性粘膜炎症。这种反应可能部分是由于防御素的失调，这是内源性产生的抗菌肽。本研究确定了microRNAs (miRNAs)是否调控α-防御素5 (DEFA5)，这可能进一步影响两者在IBD发病机制中的作用。方法:检测Caco-2细胞中DEFA5 mRNA及蛋白表达的诱导作用。计算机分析确定了DEFA5的推测miRNA结合位点。在Caco-2细胞中评估这些mirna的表达。通过荧光素酶测定这些mirna对DEFA5表达的调节。用miR-124和miR-924模拟物转染Caco-2细胞，检测DEFA5 mRNA和蛋白的表达。结果:Caco-2细胞可诱导DEFA5 mRNA及蛋白表达。在DEFA5中发现了15个推测的miRNA结合位点。诱导后miR-124和miR-924的表达降低。与转染空载体相比，转染含有DEFA5 miRNA结合位点的荧光素酶构建体导致荧光素酶活性降低。转染含有不匹配的miRNA结合位点的报告构建体导致荧光素酶活性的恢复。转染miRNA可模拟DEFA5 mRNA表达和蛋白表达的降低。结论:miR-124和miR-924负性调节DEFA5 mRNA和蛋白的表达。这些数据暗示了mirna在肠道先天免疫调节和IBD发病机制中的作用。

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引用次数: 0

Alpha-Defensin 5 Expression is Regulated by microRNAs in the Caco-2 Intestinal Epithelial Cell Line 在Caco-2肠上皮细胞系中α -防御素5的表达受microrna调控

Journal of inflammatory bowel diseases & disorders

Pub Date : 2016-04-01 DOI: 10.4172/2476-1958.1000105

D. Miles, Jun Shen, A. Chuang, Fenshi Dong, Feng Wu, J. Kwon

Background In inflammatory bowel disease (IBD), an inappropriate immune response leads to chronic mucosal inflammation. This response may be partly due to dysregulation of defensins, which are endogenously produced antimicrobial peptides. This study determined whether microRNAs (miRNAs) regulate α-defensin 5 (DEFA5), which could further implicate both in IBD pathogenesis. Methods Induction of DEFA5 mRNA and protein expression was determined in Caco-2 cells. An in silico analysis identified putative miRNA binding sites of DEFA5. Expression of these miRNAs was assessed in Caco-2 cells. Regulation of DEFA5 expression by these miRNAs was measured by luciferase assays. Caco-2 cells were transfected with miR-124 and miR-924 mimics, and DEFA5 mRNA and protein expression was measured. Results DEFA5 mRNA and protein expression was inducible in Caco-2 cells. Fifteen putative miRNA binding sites were found in DEFA5. The expression of miR-124 and miR-924 decreased following induction. Transfection of a luciferase construct containing the DEFA5 miRNA binding sites resulted in a decrease in luciferase activity compared to transfection of the empty vector. Transfection of a reporter construct containing mismatched miRNA binding sites resulted in restoration of luciferase activities. Transfection of miRNA mimics decreased DEFA5 mRNA expression and protein expression. Conclusions miR-124 and miR-924 negatively regulate DEFA5 mRNA and protein expression. These data implicate miRNAs in intestinal innate immune regulation and IBD pathogenesis.

在炎症性肠病(IBD)中，不适当的免疫反应导致慢性粘膜炎症。这种反应可能部分是由于防御素的失调，这是内源性产生的抗菌肽。本研究确定了microRNAs (miRNAs)是否调控α-防御素5 (DEFA5)，这可能进一步影响两者在IBD发病机制中的作用。方法在Caco-2细胞中检测DEFA5 mRNA和蛋白的诱导作用。计算机分析确定了DEFA5的推测miRNA结合位点。在Caco-2细胞中评估这些mirna的表达。通过荧光素酶测定这些mirna对DEFA5表达的调节。用miR-124和miR-924模拟物转染Caco-2细胞，检测DEFA5 mRNA和蛋白的表达。结果Caco-2细胞可诱导DEFA5 mRNA及蛋白表达。在DEFA5中发现了15个推测的miRNA结合位点。诱导后miR-124和miR-924的表达降低。与转染空载体相比，转染含有DEFA5 miRNA结合位点的荧光素酶构建体导致荧光素酶活性降低。转染含有不匹配的miRNA结合位点的报告构建体导致荧光素酶活性的恢复。转染miRNA可模拟DEFA5 mRNA表达和蛋白表达的降低。结论miR-124和miR-924负向调控DEFA5 mRNA和蛋白的表达。这些数据暗示了mirna在肠道先天免疫调节和IBD发病机制中的作用。

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