Porphyromonas gingivalis (P. gingivalis), the bacterial strain responsible for pathogenic changes in periodontitis, can significantly deteriorate epithelial integrity, leading to its malfunction as a protective barrier against pathogens. As one of the known intercellular adhesive proteins, E-cadherin can be affected by P. gingivalis.
Objectives
This review summarizes the most recent research on the effect of this bacterium on E-cadherin, the suggested involved mechanisms, and the contribution of this protein deterioration in the systemic disease associated with periodontitis.
Methods
In September 2024, a comprehensive search was conducted using PubMed, Scopus, Web of Science, and Google Scholar. The search focused on articles published within the last five years. Review and non-English articles were excluded. Out of 83 records found in databases, 10 records were selected for this study.
Results and conclusion
Most recent studies have consistently demonstrated the downregulation of E-cadherin in P. gingivalis-infected cells and tissues. However, there remains a need to elucidate the contribution of the bacterial infection and E-cadherin downregulation that occur during systemic diseases related to periodontitis, such as Epithelial-Mesenchymal Transition in cancer development.
背景牙龈卟啉单胞菌（P. gingivalis）是导致牙周炎致病性变化的细菌菌株，可显著破坏上皮完整性，导致其作为病原体保护屏障的功能失效。e -钙粘蛋白是一种已知的细胞间黏附蛋白，可受牙龈假单胞菌的影响。目的综述了该细菌对e -钙粘蛋白的影响、可能的机制以及该蛋白在牙周炎相关全体性疾病中的作用。方法于2024年9月，利用PubMed、Scopus、Web of Science、b谷歌Scholar进行综合检索。搜索的重点是最近五年发表的文章。综述和非英文文章被排除在外。从数据库中找到的83条记录中，选择了10条记录用于本研究。结果和结论最近的研究一致表明，E-cadherin在牙龈卟啉卟啉感染的细胞和组织中下调。然而，仍有必要阐明细菌感染和e -钙粘蛋白下调在牙周炎相关的全身性疾病中的作用，如癌症发展中的上皮-间质转化。
{"title":"Porphyromonas gingivalis modulates E-cadherin expression: a mini-review of possible involved mechanisms","authors":"Zahra Khorshidi Asl , Mahtab Mottaghi , Fatemeh Farshad , Faezeh Azmoudeh","doi":"10.1016/j.medmic.2025.100146","DOIUrl":"10.1016/j.medmic.2025.100146","url":null,"abstract":"<div><h3>Background</h3><div><em>Porphyromonas gingivalis</em> (<em>P. gingivalis</em>), the bacterial strain responsible for pathogenic changes in periodontitis, can significantly deteriorate epithelial integrity, leading to its malfunction as a protective barrier against pathogens. As one of the known intercellular adhesive proteins, E-cadherin can be affected by <em>P. gingivalis</em>.</div></div><div><h3>Objectives</h3><div>This review summarizes the most recent research on the effect of this bacterium on E-cadherin, the suggested involved mechanisms, and the contribution of this protein deterioration in the systemic disease associated with periodontitis.</div></div><div><h3>Methods</h3><div>In September 2024, a comprehensive search was conducted using PubMed, Scopus, Web of Science, and Google Scholar. The search focused on articles published within the last five years. Review and non-English articles were excluded. Out of 83 records found in databases, 10 records were selected for this study.</div></div><div><h3>Results and conclusion</h3><div>Most recent studies have consistently demonstrated the downregulation of E-cadherin in <em>P. gingivalis</em>-infected cells and tissues. However, there remains a need to elucidate the contribution of the bacterial infection and E-cadherin downregulation that occur during systemic diseases related to periodontitis, such as Epithelial-Mesenchymal Transition in cancer development.</div></div>","PeriodicalId":36019,"journal":{"name":"Medicine in Microecology","volume":"26 ","pages":"Article 100146"},"PeriodicalIF":0.0,"publicationDate":"2025-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144917710","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}
Pub Date : 2025-08-15DOI: 10.1016/j.medmic.2025.100145
Rousilândia de Araújo Silva , Igor Eduardo Silva Arruda , Maria Cidinaria Silva Alves , Ana Luiza Trajano Mangueira de Melo , Felipe de Albuquerque Marinho , José Lamartine Soares Sobrinho , Valdir de Queiroz Balbino , Cristiane Moutinho-Melo
The integration of bioinformatics and omics technologies has revolutionized leprosy research, providing insights into Mycobacterium leprae (M. leprae) biology. In this context, the present review analyzes two decades (2001–2021) of research using computational approaches to elucidate molecular mechanisms, identify biomarkers, and support drug discovery for leprosy. The search was conducted in the Web of Science database and found 30 studies, of which 23 met the inclusion criteria with a focus on genomic, proteomic and immunoinformatics applications targeting leprosy. Key advances include the identification of unique antigenic proteins, prediction of drug resistance mechanisms, and the development of in silico tools for diagnostics and therapeutic targeting. Comparative genomic studies have identified genes unique to M. leprae, such as ML2613, that may serve as potential therapeutic targets. Furthermore, bioinformatics has been used to identify biomarkers such as the recombinant antigen rMLP15, which has been shown to be effective in the diagnosis and differentiation between paucibacillary and multibacillary patients. Therefore, the present study highlights the role of bioinformatics in driving innovation for leprosy and underscores the need for continued investment in computational approaches to improve diagnostics and treatment strategies.
生物信息学和组学技术的整合彻底改变了麻风研究，为麻风分枝杆菌（M. leprae）生物学提供了见解。在此背景下，本综述分析了二十年来（2001-2021）使用计算方法阐明麻风病分子机制、识别生物标志物和支持麻风病药物发现的研究。搜索是在Web of Science数据库中进行的，发现了30项研究，其中23项符合纳入标准，重点是针对麻风病的基因组学、蛋白质组学和免疫信息学应用。主要进展包括鉴定独特的抗原蛋白，预测耐药机制，以及开发用于诊断和治疗靶向的计算机工具。比较基因组研究已经确定了麻风分枝杆菌特有的基因，如ML2613，可能作为潜在的治疗靶点。此外，生物信息学已被用于鉴定生物标志物，如重组抗原rMLP15，已被证明在诊断和区分少杆菌和多杆菌患者方面是有效的。因此，本研究强调了生物信息学在推动麻风病创新方面的作用，并强调了继续投资于计算方法以改进诊断和治疗策略的必要性。
{"title":"Bioinformatics and omics revolutionizing leprosy research: Unveiling mechanisms and driving therapeutic innovations","authors":"Rousilândia de Araújo Silva , Igor Eduardo Silva Arruda , Maria Cidinaria Silva Alves , Ana Luiza Trajano Mangueira de Melo , Felipe de Albuquerque Marinho , José Lamartine Soares Sobrinho , Valdir de Queiroz Balbino , Cristiane Moutinho-Melo","doi":"10.1016/j.medmic.2025.100145","DOIUrl":"10.1016/j.medmic.2025.100145","url":null,"abstract":"<div><div>The integration of bioinformatics and omics technologies has revolutionized leprosy research, providing insights into <em>Mycobacterium leprae</em> (<em>M. leprae</em>) biology. In this context, the present review analyzes two decades (2001–2021) of research using computational approaches to elucidate molecular mechanisms, identify biomarkers, and support drug discovery for leprosy. The search was conducted in the Web of Science database and found 30 studies, of which 23 met the inclusion criteria with a focus on genomic, proteomic and immunoinformatics applications targeting leprosy. Key advances include the identification of unique antigenic proteins, prediction of drug resistance mechanisms, and the development of <em>in silico</em> tools for diagnostics and therapeutic targeting. Comparative genomic studies have identified genes unique to <em>M. leprae</em>, such as ML2613, that may serve as potential therapeutic targets. Furthermore, bioinformatics has been used to identify biomarkers such as the recombinant antigen rMLP15, which has been shown to be effective in the diagnosis and differentiation between paucibacillary and multibacillary patients. Therefore, the present study highlights the role of bioinformatics in driving innovation for leprosy and underscores the need for continued investment in computational approaches to improve diagnostics and treatment strategies.</div></div>","PeriodicalId":36019,"journal":{"name":"Medicine in Microecology","volume":"26 ","pages":"Article 100145"},"PeriodicalIF":0.0,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144879374","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}
This study investigates the influence of zinc-mediated nutritional immunity on virulence gene expression in Uropathogenic Escherichia coli (UPEC) among female patients with recurrent urinary tract infections (UTIs). Fifty women with microbiologically confirmed UTIs were enrolled in a controlled interventional design and divided equally into zinc-supplemented and control groups. The intervention group received 40 mg elemental zinc daily for three days. Urine samples collected pre- and post-intervention were analyzed for bacterial gene expression (znuA, hlyA, fimH) using RT-qPCR, and cytokine levels (IL-6, IL-8) via ELISA. Urinary zinc levels were also quantified. The results revealed a significant increase in urinary zinc concentration following supplementation (p = 1.35 × 10−9), accompanied by marked downregulation of znuA and hlyA expression (fold changes of 0.42 and 0.53, respectively), but not fimH. Statistically significant post-intervention differences in ΔCt values for znuA and hlyA were observed only in the zinc group (p < 0.001), indicating gene-specific suppression due to zinc availability. Additionally, urinary IL-6 and IL-8 levels were significantly lower in the zinc-supplemented group (p = 1.63 × 10−5 and 4.33 × 10−12, respectively), suggesting an anti-inflammatory effect. Multivariate linear regression further identified zinc supplementation as an independent predictor of reduced IL-6 levels and increased znuA ΔCt values, while age and BMI had no significant effect on these outcomes. These findings support zinc's role in modulating both bacterial virulence and host inflammatory responses, highlighting its potential as an adjunct therapy for recurrent UTIs. By disrupting critical virulence mechanisms and reducing urinary cytokine levels, zinc supplementation may reduce the pathogenicity of UPEC and improve host outcomes. This study provides molecular and clinical insights that support dietary zinc modulation as a promising non-antibiotic strategy in managing recurrent UTIs.
{"title":"Impact of zinc-mediated nutritional immunity on uropathogenic Escherichia coli (UPEC) virulence gene expression in female recurrent UTI patients","authors":"Muthana Badeea Farhan , Areej Hamad Hassan , Hanan Hamed","doi":"10.1016/j.medmic.2025.100143","DOIUrl":"10.1016/j.medmic.2025.100143","url":null,"abstract":"<div><div>This study investigates the influence of zinc-mediated nutritional immunity on virulence gene expression in <em>Uropathogenic Escherichia coli (</em>UPEC) among female patients <u>with</u> recurrent urinary tract infections (UTIs). Fifty women with microbiologically confirmed UTIs were enrolled in a controlled interventional design and divided equally into zinc-supplemented and control groups. The intervention group received 40 mg elemental zinc daily for three days. Urine samples collected pre- and post-intervention were analyzed for bacterial gene expression (znuA, hlyA, fimH) using RT-qPCR, and cytokine levels (IL-6, IL-8) via ELISA. Urinary zinc levels were also quantified. The results revealed a significant increase in urinary zinc concentration following supplementation (p = 1.35 × 10<sup>−9</sup>), accompanied by marked downregulation of znuA and hlyA expression (fold changes of 0.42 and 0.53, respectively), but not fimH. Statistically significant post-intervention differences in ΔCt values for znuA and hlyA were observed only in the zinc group (p < 0.001), indicating gene-specific suppression due to zinc availability. Additionally, urinary IL-6 and IL-8 levels were significantly lower in the zinc-supplemented group (p = 1.63 × 10<sup>−5</sup> and 4.33 × 10<sup>−12</sup>, respectively), suggesting an anti-inflammatory effect. Multivariate linear regression further identified zinc supplementation as an independent predictor of reduced IL-6 levels and increased znuA ΔCt values, while age and BMI had no significant effect <u>on these outcomes</u>. These findings support zinc's role in modulating both bacterial virulence and host inflammatory responses, highlighting its potential as an adjunct therapy for recurrent UTIs. By disrupting critical virulence mechanisms and reducing urinary cytokine levels, zinc supplementation may reduce the pathogenicity of UPEC and improve host outcomes. This study provides molecular and clinical insights that support dietary zinc modulation as a promising non-antibiotic strategy in managing recurrent UTIs.</div></div>","PeriodicalId":36019,"journal":{"name":"Medicine in Microecology","volume":"26 ","pages":"Article 100143"},"PeriodicalIF":0.0,"publicationDate":"2025-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144865322","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}
Pub Date : 2025-08-05DOI: 10.1016/j.medmic.2025.100142
Yasir Adil Jabbar Alabdali
Enterococci have caused health problems and infections in recent years around the world, especially E. faecalis and E. faecium, due to antibiotic resistance. This study examined clinical Enterococcus isolates collected from patients at the Maternity and Children Hospital in Al-Samawah, Al-Muthanna Province, Iraq, focusing on class 1 integrons and their role in resistance. Enterococci isolated from different clinical samples were initially identified using selective medium, then confirmed using Taqman real-time PCR. A Kirby–Bauer disc diffusion test was used to determine the antibiotic susceptibility of isolates. The variable region of class 1 integrons was amplified using Polymerase Chain Reaction (PCR), and the resulting ∼2000 bp amplicons were sequenced. Sequencing analysis of VR amplification products showed the presence of three gene cassettes encoding antibiotic resistance (dhfrXII, dfrA12, aadA2). Three hundred and fifty different clinical samples were isolated between July and November 2024. The current study obtained 125 (35.7 %) enterococcal isolates divided into 35 (28 %) E. faecium and 90 (72 %) E. faecalis. Among the 125 enterococcal isolates, the int1 gene was detected in 67.2 %, and sequencing analysis of CS amplification products showed the presence of three resistance genes in this cassette (dhfrXII, dfrA12, aadA2) within clinical Enterococci, and the phylogenetic tree showed the genetic closeness with the international isolates registered in NCBI. Moreover, the antibiotic resistance and biofilm formation rates within int1-positive enterococci were noticeably higher than those lacking the int1 gene.
{"title":"Molecular characterisation of class I integrons in clinical multidrug-resistant Enterococcus spp.","authors":"Yasir Adil Jabbar Alabdali","doi":"10.1016/j.medmic.2025.100142","DOIUrl":"10.1016/j.medmic.2025.100142","url":null,"abstract":"<div><div><em>Enterococci</em> have caused health problems and infections in recent years around the world, especially <em>E. faecalis and E. faecium</em>, due to antibiotic resistance. This study examined clinical <em>Enterococcus</em> isolates collected from patients at the Maternity and Children Hospital in Al-Samawah, Al-Muthanna Province, Iraq, focusing on class 1 integrons and their role in resistance. Enterococci isolated from different clinical samples were initially identified using selective medium, then confirmed using Taqman real-time PCR. A Kirby–Bauer disc diffusion test was used to determine the antibiotic susceptibility of isolates. The variable region of class 1 integrons was amplified using Polymerase Chain Reaction (PCR), and the resulting ∼2000 bp amplicons were sequenced. Sequencing analysis of VR amplification products showed the presence of three gene cassettes encoding antibiotic resistance (<em>dhfrXII, dfrA12, aadA2</em>). Three hundred and fifty different clinical samples were isolated between July and November 2024. The current study obtained 125 (35.7 %) enterococcal isolates divided into 35 (28 %) <em>E. faecium</em> and 90 (72 %) <em>E. faecalis</em>. Among the 125 enterococcal isolates, the <em>int</em>1 gene was detected in 67.2 %, and sequencing analysis of CS amplification products showed the presence of three resistance genes in this cassette (<em>dhfrXII, dfrA12, aadA2</em>) within clinical <em>Enterococci</em>, and the phylogenetic tree showed the genetic closeness with the international isolates registered in NCBI. Moreover, the antibiotic resistance and biofilm formation rates within int1-positive enterococci were noticeably higher than those lacking the int1 gene.</div></div>","PeriodicalId":36019,"journal":{"name":"Medicine in Microecology","volume":"26 ","pages":"Article 100142"},"PeriodicalIF":0.0,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144830569","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}
Pub Date : 2025-07-26DOI: 10.1016/j.medmic.2025.100141
Adriana Alejandra Márquez Ibarra, Laura Fernanda Barrera Hernández, Edith Valbuena Gregorio, Francisco Javier Olivas Aguirre, Jael Teresa de Jesús Quintero Vargas
Metabolic adaptations are essential for achieving a healthy full-term pregnancy. These changes are influenced by the maternal microbiota, specifically its composition and diversity, which are, in turn, shaped by the physiological demands of pregnancy. This review examines scientific evidence on the role of the microbiota during pregnancy, childbirth, and the postpartum period, and its association with both health and disease states. Notable microbiota shifts during pregnancy include changes in the vaginal microbiota (with a predominance of Lactobacillus species), the gastrointestinal tract (increased levels of Proteobacteria and Actinobacteria), the oral cavity (higher prevalence of bacteria such as Aggregatibacter actinomycetemcomitans), and breast milk (presence of Lactobacillus spp.). Disruption of microbial homeostasis (dysbiosis) during pregnancy has been linked to a variety of obstetric, fetal, and neonatal complications, including gestational diabetes, preeclampsia, intrauterine growth restriction, low birth weight, and preterm birth. Multiple studies have documented the role of diet in the development of dysbiosis and its connection to mental health disorders. Diets high in saturated fats appear to significantly influence gut microbiota due to their pro-inflammatory effects. Additionally, low fiber intake has been associated with reduced microbial diversity and an increased abundance of Collinsella, a genus linked to type 2 diabetes. Therefore, dietary interventions aimed at enhancing microbial balance and reducing systemic inflammation are recommended. A multidisciplinary approach is also crucial for translating current findings into clinical strategies, particularly for populations at increased risk.
{"title":"Microbiota during pregnancy, childbirth, and postpartum, and its relationship with health and disease states","authors":"Adriana Alejandra Márquez Ibarra, Laura Fernanda Barrera Hernández, Edith Valbuena Gregorio, Francisco Javier Olivas Aguirre, Jael Teresa de Jesús Quintero Vargas","doi":"10.1016/j.medmic.2025.100141","DOIUrl":"10.1016/j.medmic.2025.100141","url":null,"abstract":"<div><div>Metabolic adaptations are essential for achieving a healthy full-term pregnancy. These changes are influenced by the maternal microbiota, specifically its composition and diversity, which are, in turn, shaped by the physiological demands of pregnancy. This review examines scientific evidence on the role of the microbiota during pregnancy, childbirth, and the postpartum period, and its association with both health and disease states. Notable microbiota shifts during pregnancy include changes in the vaginal microbiota (with a predominance of <em>Lactobacillus</em> species), the gastrointestinal tract (increased levels of <em>Proteobacteria</em> and <em>Actinobacteria</em>), the oral cavity (higher prevalence of bacteria such as <em>Aggregatibacter actinomycetemcomitans</em>), and breast milk (presence of <em>Lactobacillus</em> spp.). Disruption of microbial homeostasis (dysbiosis) during pregnancy has been linked to a variety of obstetric, fetal, and neonatal complications, including gestational diabetes, preeclampsia, intrauterine growth restriction, low birth weight, and preterm birth. Multiple studies have documented the role of diet in the development of dysbiosis and its connection to mental health disorders. Diets high in saturated fats appear to significantly influence gut microbiota due to their pro-inflammatory effects. Additionally, low fiber intake has been associated with reduced microbial diversity and an increased abundance of <em>Collinsella</em>, a genus linked to type 2 diabetes. Therefore, dietary interventions aimed at enhancing microbial balance and reducing systemic inflammation are recommended. A multidisciplinary approach is also crucial for translating current findings into clinical strategies, particularly for populations at increased risk.</div></div>","PeriodicalId":36019,"journal":{"name":"Medicine in Microecology","volume":"25 ","pages":"Article 100141"},"PeriodicalIF":0.0,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144739708","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}
Pub Date : 2025-07-21DOI: 10.1016/j.medmic.2025.100140
Zaid Mohammed Joodi Al-Janabi , Waseem Yousif M. Al-dulaimy , Maryam Hekmat Abdulateef , Aeshah Abbood Ahmed , Mohammed Kadhom
The present study describes the green synthesis of silver nanoparticles (AgNPs) using a glycolipopeptide (GLP) biosurfactant produced by Lactobacillus plantarum, and evaluates their physicochemical characteristics and anticancer potential. The formation of AgNPs was visually confirmed by a color change and further characterized by UV–Vis, XRD, AFM, and TEM, revealing spherical particles ranging from 20 to 300 nm. Zeta potential analysis (−32.1 mV) confirmed strong colloidal stability. FTIR and GC-MS analyses identified key functional groups and bioactive compounds in the GLP, including fatty acids and lipopeptides responsible for both surface activity and biological effects. Surface tension (32.4 mN/m) and emulsification index (61.5 %) further validated the biosurfactant's amphiphilic nature. In vitro cytotoxicity assays against MCF-7 breast cancer cells demonstrated dose-dependent effects, with the GLP and AgNPs showing 60.59 % and 54.77 % inhibition, respectively, at 400 μg/mL. Their combination enhanced cytotoxicity to 69.14 % while maintaining minimal toxicity toward WRL-68 normal liver cells, indicating selective activity. Compared to doxorubicin (IC50 ≈ 0.98 μg/mL, SI ≈ 1.01), the green formulations displayed a higher selectivity index (SI ≈ 2.71). The enhanced cytotoxicity is likely attributed to reactive oxygen species (ROS) generation, apoptosis induction, and membrane disruption. Although our findings highlight the dual functionality of the GLP biosurfactant as both a nanoparticle stabilizer and a bioactive agent, further in vivo studies and mechanistic investigations are warranted to validate its potential in cancer therapy.
{"title":"Comparative cytotoxicity of a glycolipopeptide biosurfactant from Lactobacillus plantarum and its derived silver nanoparticles against breast cancer cells","authors":"Zaid Mohammed Joodi Al-Janabi , Waseem Yousif M. Al-dulaimy , Maryam Hekmat Abdulateef , Aeshah Abbood Ahmed , Mohammed Kadhom","doi":"10.1016/j.medmic.2025.100140","DOIUrl":"10.1016/j.medmic.2025.100140","url":null,"abstract":"<div><div>The present study describes the green synthesis of silver nanoparticles (AgNPs) using a glycolipopeptide (GLP) biosurfactant produced by <em>Lactobacillus plantarum</em>, and evaluates their physicochemical characteristics and anticancer potential. The formation of AgNPs was visually confirmed by a color change and further characterized by UV–Vis, XRD, AFM, and TEM, revealing spherical particles ranging from 20 to 300 nm. Zeta potential analysis (−32.1 mV) confirmed strong colloidal stability. FTIR and GC-MS analyses identified key functional groups and bioactive compounds in the GLP, including fatty acids and lipopeptides responsible for both surface activity and biological effects. Surface tension (32.4 mN/m) and emulsification index (61.5 %) further validated the biosurfactant's amphiphilic nature. In vitro cytotoxicity assays against MCF-7 breast cancer cells demonstrated dose-dependent effects, with the GLP and AgNPs showing 60.59 % and 54.77 % inhibition, respectively, at 400 μg/mL. Their combination enhanced cytotoxicity to 69.14 % while maintaining minimal toxicity toward WRL-68 normal liver cells, indicating selective activity. Compared to doxorubicin (IC<sub>50</sub> ≈ 0.98 μg/mL, SI ≈ 1.01), the green formulations displayed a higher selectivity index (SI ≈ 2.71). The enhanced cytotoxicity is likely attributed to reactive oxygen species (ROS) generation, apoptosis induction, and membrane disruption. Although our findings highlight the dual functionality of the GLP biosurfactant as both a nanoparticle stabilizer and a bioactive agent, further in vivo studies and mechanistic investigations are warranted to validate its potential in cancer therapy.</div></div>","PeriodicalId":36019,"journal":{"name":"Medicine in Microecology","volume":"25 ","pages":"Article 100140"},"PeriodicalIF":0.0,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144749134","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}
Pub Date : 2025-07-10DOI: 10.1016/j.medmic.2025.100139
P. Sankarganesh , Adrija Bhunia , A. Ganesh Kumar , A. Surendra Babu , S.T. Gopukumar , E. Lokesh
Short-chain fatty acids (SCFAs) are the primary energy substrate for colonocytes, synthesized in the gut when gut microbiomes ferment the dietary fibers. SCFAs play crucial roles in maintaining gut homeostasis and exerting systemic effects beyond the gastrointestinal tract. Liver disorders, cardiovascular, diabetes, and obesity like metabolic syndromes are strongly associated with these metabolites’ imbalance. Determining the genetic variability, diet-gene interactions, and microbiome diversity in SCFA production is essential for creation of targeted interventions to optimize gut health and mitigate disease risk. The present review aims to elucidate the nutrigenomics and nitrogenic analysis to improve SCFAs to modulate intestinal barrier function, regulate immune responses, and influence host metabolism. This review summarizes deep insights into the multifaceted functions of SCFAs, therapeutic potential of SCFAs in promoting a thriving gut system and overall health and their involvement in neurological and metabolic disorders, highlighting the complex mechanism between gut microbiota and systemic health. A model was proposed to produce resistant starch as source of SCFAs production. The specific bacteria involved in SCFAs production and their functions also discussed. In addition to outlining the potential benefits of SCFAs for human health, it specified the factors influencing and obstacles to this field of study and offered suggestions for future research directions.
{"title":"Short-chain fatty acids (SCFAs) in gut health: Implications for drug metabolism and therapeutics","authors":"P. Sankarganesh , Adrija Bhunia , A. Ganesh Kumar , A. Surendra Babu , S.T. Gopukumar , E. Lokesh","doi":"10.1016/j.medmic.2025.100139","DOIUrl":"10.1016/j.medmic.2025.100139","url":null,"abstract":"<div><div>Short-chain fatty acids (SCFAs) are the primary energy substrate for colonocytes, synthesized in the gut when gut microbiomes ferment the dietary fibers. SCFAs play crucial roles in maintaining gut homeostasis and exerting systemic effects beyond the gastrointestinal tract. Liver disorders, cardiovascular, diabetes, and obesity like metabolic syndromes are strongly associated with these metabolites’ imbalance. Determining the genetic variability, diet-gene interactions, and microbiome diversity in SCFA production is essential for creation of targeted interventions to optimize gut health and mitigate disease risk. The present review aims to elucidate the nutrigenomics and nitrogenic analysis to improve SCFAs to modulate intestinal barrier function, regulate immune responses, and influence host metabolism. This review summarizes deep insights into the multifaceted functions of SCFAs, therapeutic potential of SCFAs in promoting a thriving gut system and overall health and their involvement in neurological and metabolic disorders, highlighting the complex mechanism between gut microbiota and systemic health. A model was proposed to produce resistant starch as source of SCFAs production. The specific bacteria involved in SCFAs production and their functions also discussed. In addition to outlining the potential benefits of SCFAs for human health, it specified the factors influencing and obstacles to this field of study and offered suggestions for future research directions.</div></div>","PeriodicalId":36019,"journal":{"name":"Medicine in Microecology","volume":"25 ","pages":"Article 100139"},"PeriodicalIF":0.0,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144631631","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}
Pub Date : 2025-06-27DOI: 10.1016/j.medmic.2025.100138
Tanushree D. Malode , Pranali Chandurkar , Brijesh G. Taksande , Amol A. Tatode , Mohammad Qutub , Tanvi Premchandani , Milind J. Umekar , Jayshree B. Taksande
Autism Spectrum Disorder (ASD) is a complex neurodevelopmental condition characterized by social communication deficits and restrictive, repetitive behaviors. A significant proportion of individuals with ASD also suffer from anxiety disorders, further compounding their behavioral and emotional challenges. Conventional therapies for anxiety in ASD, including pharmacological and behavioral interventions, often yield suboptimal results and carry notable limitations. Growing research highlights the critical role of the gut-brain axis in neurodevelopment and emotional regulation, with gut microbiota dysbiosis increasingly implicated in both ASD and anxiety pathogenesis. Faecal microbiota transplantation (FMT), a therapeutic approach aimed at restoring microbial homeostasis by transferring fecal material from healthy donors, has emerged as a novel intervention of interest. Preclinical studies have demonstrated that alterations in gut microbiota can modulate social behaviors and anxiety-like symptoms, with FMT reversing many pathological features in animal models. Early clinical investigations, though limited, suggest that FMT may improve gastrointestinal health, core ASD symptoms, and comorbid anxiety. Mechanistically, FMT is thought to reduce neuroinflammation, restore neurotransmitter balance, and normalize stress responses by enhancing gut microbial diversity and metabolic function. However, significant challenges remain, including concerns about safety, standardization, donor selection, and regulatory approval. Future research must focus on large-scale, controlled trials and the identification of biomarkers predictive of FMT response to establish its therapeutic potential more conclusively. This review critically examines the existing evidence, explores the mechanistic pathways linking gut microbiota to anxiety in ASD, and discusses the future directions necessary to translate FMT into a viable clinical strategy for autism-associated anxiety.
{"title":"Faecal microbiota transplantation as a novel approach for autism-associated anxiety: A critical therapeutic appraisal","authors":"Tanushree D. Malode , Pranali Chandurkar , Brijesh G. Taksande , Amol A. Tatode , Mohammad Qutub , Tanvi Premchandani , Milind J. Umekar , Jayshree B. Taksande","doi":"10.1016/j.medmic.2025.100138","DOIUrl":"10.1016/j.medmic.2025.100138","url":null,"abstract":"<div><div>Autism Spectrum Disorder (ASD) is a complex neurodevelopmental condition characterized by social communication deficits and restrictive, repetitive behaviors. A significant proportion of individuals with ASD also suffer from anxiety disorders, further compounding their behavioral and emotional challenges. Conventional therapies for anxiety in ASD, including pharmacological and behavioral interventions, often yield suboptimal results and carry notable limitations. Growing research highlights the critical role of the gut-brain axis in neurodevelopment and emotional regulation, with gut microbiota dysbiosis increasingly implicated in both ASD and anxiety pathogenesis. Faecal microbiota transplantation (FMT), a therapeutic approach aimed at restoring microbial homeostasis by transferring fecal material from healthy donors, has emerged as a novel intervention of interest. Preclinical studies have demonstrated that alterations in gut microbiota can modulate social behaviors and anxiety-like symptoms, with FMT reversing many pathological features in animal models. Early clinical investigations, though limited, suggest that FMT may improve gastrointestinal health, core ASD symptoms, and comorbid anxiety. Mechanistically, FMT is thought to reduce neuroinflammation, restore neurotransmitter balance, and normalize stress responses by enhancing gut microbial diversity and metabolic function. However, significant challenges remain, including concerns about safety, standardization, donor selection, and regulatory approval. Future research must focus on large-scale, controlled trials and the identification of biomarkers predictive of FMT response to establish its therapeutic potential more conclusively. This review critically examines the existing evidence, explores the mechanistic pathways linking gut microbiota to anxiety in ASD, and discusses the future directions necessary to translate FMT into a viable clinical strategy for autism-associated anxiety.</div></div>","PeriodicalId":36019,"journal":{"name":"Medicine in Microecology","volume":"25 ","pages":"Article 100138"},"PeriodicalIF":0.0,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144523440","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}
Today, probiotics are one of the most popular microbial groups for the development of research due to their naturalness and beneficial health effects. Recently, next-generation probiotics (NGPs), with the emerging concept of live biotherapeutic products have been proposed. Bacteroides and especially Bacteroides fragilis, as a potent NGP, is one of the members of the gut microbiota and, like a double-edged sword, plays a role in both causing diseases such as colitis, colorectal cancer, and Alzheimer's, and in preventing and improving diseases such as colitis, cancer, central nervous system disorders, infectious diseases, asthma, and abscesses. In fact, certain strains of B. fragilis have been found to exert beneficial effects on the host. Therefore, our aim in this study was to review and summarize the role and metabolic status of B. fragilis in the body, focusing on its immunomodulatory and beneficial effects.
{"title":"The metabolic and immunomodulatory functions of Bacteroides fragilis; a next-generation probiotic?","authors":"Roya Roustapoor , Elmira Abdi , Atiye Khabbaz , Armin Abdi","doi":"10.1016/j.medmic.2025.100137","DOIUrl":"10.1016/j.medmic.2025.100137","url":null,"abstract":"<div><div>Today, probiotics are one of the most popular microbial groups for the development of research due to their naturalness and beneficial health effects. Recently, next-generation probiotics (NGPs), with the emerging concept of live biotherapeutic products have been proposed. <em>Bacteroides</em> and especially <em>Bacteroides fragilis</em>, as a potent NGP, is one of the members of the gut microbiota and, like a double-edged sword, plays a role in both causing diseases such as colitis, colorectal cancer, and Alzheimer's, and in preventing and improving diseases such as colitis, cancer, central nervous system disorders, infectious diseases, asthma, and abscesses. In fact, certain strains of <em>B. fragilis</em> have been found to exert beneficial effects on the host. Therefore, our aim in this study was to review and summarize the role and metabolic status of <em>B. fragilis</em> in the body, focusing on its immunomodulatory and beneficial effects.</div></div>","PeriodicalId":36019,"journal":{"name":"Medicine in Microecology","volume":"25 ","pages":"Article 100137"},"PeriodicalIF":0.0,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144321466","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}
Pub Date : 2025-06-12DOI: 10.1016/j.medmic.2025.100136
Neha Jaiswal, Awanish Kumar
Candida albicans is a significant opportunistic fungal pathogen known for its virulence and capacity to develop multidrug resistance (MDR), complicating treatment efforts. Its pathogenicity is driven by factors such as adhesion to host tissues, morphological switching between yeast and filamentous forms, biofilm formation, and the secretion of hydrolytic enzymes. These mechanisms allow C. albicans to evade the host immune response, persist on medical devices, and resist available antifungal treatments. In our study, we investigated the CAP1 protein as a potent therapeutic target due to its critical role in these processes. Further, we identified its localization, and it was found that CAP1 is located in the cytoplasm, which further makes it a viable drug target. The gene ontology analysis reveals that CAP1 is involved in crucial cellular functions, including metabolism and regulation, suggesting that inhibiting CAP1 could disrupt essential processes. Our findings reveal that CAP1 is expressed in both planktonic, hyphal, and biofilm stages of C. albicans, playing a pivotal role in the transition from planktonic to hyphal and biofilm states. The interaction analysis via string database and Cytoscape highlights the extensive protein-protein interaction network centred around CAP1. This network includes key proteins such as ALS3, HWP1, TUP1, SAP4, and others involved in MDR, like MRR1, MDR2, CDR1, and biofilm formation. CAP1's interactions with these proteins suggest its crucial role in phase switching, regulating virulence, and pathogenicity. The identification of CAP1 as a central hub protein within this network underscores its significance in the regulation of MDR and biofilm formation of C. albicans, which highlights its potential as a promising futuristic target for the development of effective antifungal agents.
{"title":"Deciphering CAP1 of Candida albicans as a key druggable target protein","authors":"Neha Jaiswal, Awanish Kumar","doi":"10.1016/j.medmic.2025.100136","DOIUrl":"10.1016/j.medmic.2025.100136","url":null,"abstract":"<div><div><em>Candida albicans</em> is a significant opportunistic fungal pathogen known for its virulence and capacity to develop multidrug resistance (MDR), complicating treatment efforts. Its pathogenicity is driven by factors such as adhesion to host tissues, morphological switching between yeast and filamentous forms, biofilm formation, and the secretion of hydrolytic enzymes. These mechanisms allow <em>C. albicans</em> to evade the host immune response, persist on medical devices, and resist available antifungal treatments. In our study, we investigated the CAP1 protein as a potent therapeutic target due to its critical role in these processes. Further, we identified its localization, and it was found that CAP1 is located in the cytoplasm, which further makes it a viable drug target. The gene ontology analysis reveals that CAP1 is involved in crucial cellular functions, including metabolism and regulation, suggesting that inhibiting CAP1 could disrupt essential processes. Our findings reveal that CAP1 is expressed in both planktonic, hyphal, and biofilm stages of <em>C. albicans</em>, playing a pivotal role in the transition from planktonic to hyphal and biofilm states. The interaction analysis via string database and Cytoscape highlights the extensive protein-protein interaction network centred around CAP1. This network includes key proteins such as ALS3, HWP1, TUP1, SAP4, and others involved in MDR, like MRR1, MDR2, CDR1, and biofilm formation. CAP1's interactions with these proteins suggest its crucial role in phase switching, regulating virulence, and pathogenicity. The identification of CAP1 as a central hub protein within this network underscores its significance in the regulation of MDR and biofilm formation of <em>C. albicans</em>, which highlights its potential as a promising futuristic target for the development of effective antifungal agents.</div></div>","PeriodicalId":36019,"journal":{"name":"Medicine in Microecology","volume":"25 ","pages":"Article 100136"},"PeriodicalIF":0.0,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144321465","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}
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