F. Mohammadi, Amirhossein Gholamlou, M. Mirzadeh, Z. Ghasemi, Hadi Aliyari
{"title":"In Vitro Enzymatic Virulence Factors of Dermatophytes Species Isolated From Clinical Specimens","authors":"F. Mohammadi, Amirhossein Gholamlou, M. Mirzadeh, Z. Ghasemi, Hadi Aliyari","doi":"10.32598/jid.26.1.8","DOIUrl":"https://doi.org/10.32598/jid.26.1.8","url":null,"abstract":"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.","PeriodicalId":91544,"journal":{"name":"Journal of inflammatory bowel diseases & disorders","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89472101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Association of Sleep Quality and Duration With Preterm Birth: The Qazvin Maternal and Neonatal Metabolic Study (QMNMS)","authors":"S. Hashemipour, F. Lalooha, Khadijeh Elmizadeh","doi":"10.32598/jid.26.1.9","DOIUrl":"https://doi.org/10.32598/jid.26.1.9","url":null,"abstract":"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.","PeriodicalId":91544,"journal":{"name":"Journal of inflammatory bowel diseases & disorders","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81807692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Telomere Dysfunction as an Initiator of Inflammation: Clues to an Age-Old Mystery.","authors":"Deepavali Chakravarti, Ronald A DePinho","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":91544,"journal":{"name":"Journal of inflammatory bowel diseases & disorders","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8516314/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39530141","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Donald R B Miles, Jun Shen, Alice Y Chuang, Fenshi Dong, Feng Wu, John Kwon
{"title":"Alpha-Defensin 5 Expression is Regulated by microRNAs in the Caco-2 Intestinal Epithelial Cell Line.","authors":"Donald R B Miles, Jun Shen, Alice Y Chuang, Fenshi Dong, Feng Wu, John Kwon","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>Induction of DEFA5 mRNA and protein expression was determined in Caco-2 cells. An <i>in silico</i> 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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusions: </strong>miR-124 and miR-924 negatively regulate DEFA5 mRNA and protein expression. These data implicate miRNAs in intestinal innate immune regulation and IBD pathogenesis.</p>","PeriodicalId":91544,"journal":{"name":"Journal of inflammatory bowel diseases & disorders","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4979555/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34307477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
D. Miles, Jun Shen, A. Chuang, Fenshi Dong, Feng Wu, J. Kwon
{"title":"Alpha-Defensin 5 Expression is Regulated by microRNAs in the Caco-2 Intestinal Epithelial Cell Line","authors":"D. Miles, Jun Shen, A. Chuang, Fenshi Dong, Feng Wu, J. Kwon","doi":"10.4172/2476-1958.1000105","DOIUrl":"https://doi.org/10.4172/2476-1958.1000105","url":null,"abstract":"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.","PeriodicalId":91544,"journal":{"name":"Journal of inflammatory bowel diseases & disorders","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77845341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}