Pub Date : 2025-10-25DOI: 10.1016/j.medmic.2025.100156
Amruta A. Joshi, Ravindra H. Patil
Due to biofilms' unique ability to protect bacteria from antibiotics and host immune responses, biofilm-associated infections continue to be a persistent problem and are at the core of the rise in antimicrobial resistance (AMR). Structured microbial communities called biofilms, which are surrounded by an extracellular polymeric matrix that the bacteria manufacture on their own, can increase bacterial resistance to therapy by up to 1000 times. This protected environment promotes the horizontal transfer of resistance genes in addition to impeding medication efficacy. Nanoparticles (NPs) have become a promising weapon in the fight against biofilms in recent years. They can break down structural integrity, improve antibiotic delivery, and penetrate biofilm matrices because of their unique physicochemical characteristics. This review article highlights the classes of NPs used as anti-biofilm agents —such as metal and metal oxide nanoparticles, polymeric nanocarriers, and lipid-based systems sheds light on their mechanisms of action, including reactive oxygen species (ROS) generation, inhibition of quorum sensing, degradation of biofilm matrix, and enhanced drug permeability. Finally, the challenges in the clinical application of NPs such as nanotoxicity, environmental issues, practical applications and future directions are discussed.
{"title":"Nanoparticles targeting biofilms: A new era in combating antimicrobial resistance","authors":"Amruta A. Joshi, Ravindra H. Patil","doi":"10.1016/j.medmic.2025.100156","DOIUrl":"10.1016/j.medmic.2025.100156","url":null,"abstract":"<div><div>Due to biofilms' unique ability to protect bacteria from antibiotics and host immune responses, biofilm-associated infections continue to be a persistent problem and are at the core of the rise in antimicrobial resistance (AMR). Structured microbial communities called biofilms, which are surrounded by an extracellular polymeric matrix that the bacteria manufacture on their own, can increase bacterial resistance to therapy by up to 1000 times. This protected environment promotes the horizontal transfer of resistance genes in addition to impeding medication efficacy. Nanoparticles (NPs) have become a promising weapon in the fight against biofilms in recent years. They can break down structural integrity, improve antibiotic delivery, and penetrate biofilm matrices because of their unique physicochemical characteristics. This review article highlights the classes of NPs used as anti-biofilm agents —such as metal and metal oxide nanoparticles, polymeric nanocarriers, and lipid-based systems sheds light on their mechanisms of action, including reactive oxygen species (ROS) generation, inhibition of quorum sensing, degradation of biofilm matrix, and enhanced drug permeability. Finally, the challenges in the clinical application of NPs such as nanotoxicity, environmental issues, practical applications and future directions are discussed.</div></div>","PeriodicalId":36019,"journal":{"name":"Medicine in Microecology","volume":"26 ","pages":"Article 100156"},"PeriodicalIF":0.0,"publicationDate":"2025-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145424434","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}
The nasal and gut microbiomes are recognised as key regulators of mucosal and systemic immunity. While each has been studied extensively in isolation, evidence suggests they are connected through a bidirectional network of immune signalling, microbial metabolites, and barrier integrity, forming what may be termed “the nasal–gut microbiome axis”. This review synthesises current knowledge on the composition and function of these microbiomes, highlighting shared features, environmental influences, and patterns of dysbiosis observed in conditions such as asthma, allergic rhinitis, and chronic rhinosinusitis. We examine potential mechanisms of cross-talk, including cytokine and chemokine exchange, short-chain fatty acid mediated epigenetic regulation, and dendritic cell–driven immune priming across mucosal sites. Clinical implications are explored, with particular attention to dual-site microbiome modulation strategies, concurrent nasal–gut microbial profiling for diagnostics, and microbiome-informed precision therapies. Despite promising early evidence, knowledge gaps persist, particularly the scarcity of longitudinal, multi-omic studies and mechanistic human data. Framing the nasal and gut microbiomes as components of an integrated mucosal network, this review aims to advance understanding of their connection, and encourage research that could transform prevention and treatment strategies for immune-mediated respiratory disease.
{"title":"Nasal-gut microbiome axis in health and disease","authors":"Jude Oluwapelumi Alao , Favour Oluwadara Bamigboye","doi":"10.1016/j.medmic.2025.100153","DOIUrl":"10.1016/j.medmic.2025.100153","url":null,"abstract":"<div><div>The nasal and gut microbiomes are recognised as key regulators of mucosal and systemic immunity. While each has been studied extensively in isolation, evidence suggests they are connected through a bidirectional network of immune signalling, microbial metabolites, and barrier integrity, forming what may be termed “the nasal–gut microbiome axis”. This review synthesises current knowledge on the composition and function of these microbiomes, highlighting shared features, environmental influences, and patterns of dysbiosis observed in conditions such as asthma, allergic rhinitis, and chronic rhinosinusitis. We examine potential mechanisms of cross-talk, including cytokine and chemokine exchange, short-chain fatty acid mediated epigenetic regulation, and dendritic cell–driven immune priming across mucosal sites. Clinical implications are explored, with particular attention to dual-site microbiome modulation strategies, concurrent nasal–gut microbial profiling for diagnostics, and microbiome-informed precision therapies. Despite promising early evidence, knowledge gaps persist, particularly the scarcity of longitudinal, multi-omic studies and mechanistic human data. Framing the nasal and gut microbiomes as components of an integrated mucosal network, this review aims to advance understanding of their connection, and encourage research that could transform prevention and treatment strategies for immune-mediated respiratory disease.</div></div>","PeriodicalId":36019,"journal":{"name":"Medicine in Microecology","volume":"26 ","pages":"Article 100153"},"PeriodicalIF":0.0,"publicationDate":"2025-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145424436","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 : 2025-10-19DOI: 10.1016/j.medmic.2025.100155
Haja Abdul Nazeer , Suganya Kannan , Jeyakumar Balakrishanan , Vijaya Kumar Nair , Y. Kavitha , Namrata K. Bhosale
Breast cancer remains a major global health concern, with persistent challenges in recurrence, treatment resistance, and therapy-related toxicity. Parallel to advancements in oncology, recent research has uncovered a compelling connection between the gut microbiota and breast cancer pathogenesis, progression, and therapeutic response. This comprehensive review synthesizes current evidence linking microbial dysbiosis to breast cancer through key mechanisms such as chronic systemic inflammation, estrogen metabolism via the estrobolome, genotoxin production, immune system modulation, and epigenetic alterations. The emerging concept of the gut-mammary axis illustrates a systemic interplay whereby gut-derived microbial metabolites and immune signals directly influence breast tissue and tumor biology. Additionally, specific microbial profiles have been shown to impact the efficacy and toxicity of chemotherapy and immune checkpoint inhibitors, opening new avenues for microbiome-targeted interventions. With growing interest in personalized nutrition, probiotics, and fecal microbiota transplantation, the gut microbiota is poised to become an integral component of precision oncology. This review highlights the translational potential of microbiome science in breast cancer prevention, prognosis, and therapy, while calling for rigorous interdisciplinary research and large-scale clinical trials to validate and integrate these findings into standard care.
{"title":"The gut microbiota and breast cancer: A comprehensive review of emerging links and therapeutic implications","authors":"Haja Abdul Nazeer , Suganya Kannan , Jeyakumar Balakrishanan , Vijaya Kumar Nair , Y. Kavitha , Namrata K. Bhosale","doi":"10.1016/j.medmic.2025.100155","DOIUrl":"10.1016/j.medmic.2025.100155","url":null,"abstract":"<div><div>Breast cancer remains a major global health concern, with persistent challenges in recurrence, treatment resistance, and therapy-related toxicity. Parallel to advancements in oncology, recent research has uncovered a compelling connection between the gut microbiota and breast cancer pathogenesis, progression, and therapeutic response. This comprehensive review synthesizes current evidence linking microbial dysbiosis to breast cancer through key mechanisms such as chronic systemic inflammation, estrogen metabolism via the estrobolome, genotoxin production, immune system modulation, and epigenetic alterations. The emerging concept of the gut-mammary axis illustrates a systemic interplay whereby gut-derived microbial metabolites and immune signals directly influence breast tissue and tumor biology. Additionally, specific microbial profiles have been shown to impact the efficacy and toxicity of chemotherapy and immune checkpoint inhibitors, opening new avenues for microbiome-targeted interventions. With growing interest in personalized nutrition, probiotics, and fecal microbiota transplantation, the gut microbiota is poised to become an integral component of precision oncology. This review highlights the translational potential of microbiome science in breast cancer prevention, prognosis, and therapy, while calling for rigorous interdisciplinary research and large-scale clinical trials to validate and integrate these findings into standard care.</div></div>","PeriodicalId":36019,"journal":{"name":"Medicine in Microecology","volume":"26 ","pages":"Article 100155"},"PeriodicalIF":0.0,"publicationDate":"2025-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145424435","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}
Alcoholic liver disease (ALD) remains a major global health burden driven by chronic alcohol consumption and characterized by progressive liver injury, inflammation, and fibrosis. A growing body of evidence highlights the central role of the gut-liver axis in ALD pathogenesis, where alcohol-induced dysbiosis and intestinal barrier disruption facilitate the translocation of bacterial endotoxins such as lipopolysaccharides (LPS) into the liver. These microbial products activate Kupffer cells via Toll-like receptor 4 (TLR4) signaling, triggering inflammatory cascades, oxidative stress, and hepatic stellate cell activation, thereby promoting fibrogenesis. Dysregulated bile acid metabolism, impaired FXR and TGR5 signaling, and depletion of beneficial microbial metabolites such as short-chain fatty acids (SCFAs) further contribute to liver damage. Advances in metabolomics have uncovered distinct microbial and host-derived metabolic signatures linked to disease severity, including SCFA depletion, elevated trimethylamine-N-oxide (TMAO), and bile acid imbalances. Precision interventions targeting the gut microbiota—such as probiotics, prebiotics, synbiotics, and microbial metabolite supplementation—are showing promise in modulating gut-liver interactions and mitigating ALD progression. Furthermore, the integration of multi-omics datasets with artificial intelligence (AI)-driven models is paving the way for personalized treatment strategies based on individual microbiome-metabolome profiles. This review consolidates current insights into ALD pathogenesis, the gut-liver axis, and emerging microbiota-centered precision therapies that are reshaping the future of ALD management.
酒精性肝病（ALD）仍然是由慢性饮酒引起的主要全球健康负担，其特征是进行性肝损伤、炎症和纤维化。越来越多的证据强调了肠-肝轴在ALD发病机制中的核心作用，其中酒精诱导的生态失调和肠屏障破坏促进了细菌内毒素（如脂多糖（LPS））转运到肝脏。这些微生物产物通过toll样受体4 （TLR4）信号激活库普弗细胞，引发炎症级联反应、氧化应激和肝星状细胞活化，从而促进纤维形成。胆汁酸代谢失调、FXR和TGR5信号通路受损以及有益微生物代谢物如短链脂肪酸（SCFAs）的消耗进一步导致肝损伤。代谢组学的进展揭示了与疾病严重程度相关的不同微生物和宿主来源的代谢特征，包括SCFA消耗、三甲胺- n -氧化物（TMAO）升高和胆酸失衡。针对肠道微生物群的精确干预，如益生菌、益生元、合成菌和微生物代谢物补充，在调节肠-肝相互作用和减缓ALD进展方面显示出希望。此外，将多组学数据集与人工智能（AI）驱动的模型相结合，为基于个体微生物组代谢组谱的个性化治疗策略铺平了道路。这篇综述整合了目前对ALD发病机制、肠-肝轴和新兴的以微生物群为中心的精确疗法的见解，这些疗法正在重塑ALD管理的未来。
{"title":"Understanding the interconnected roles of gut microbiota and metabolomic profiles in alcoholic liver disease pathophysiology and their potential for innovative treatment strategies","authors":"Jeyakumar Balakrishnan , Suganya Kannan , Ganeshbala Arivazhagan , Niranjjan Ramachandran , Vanitha Gnanasoundran Sundarasamy","doi":"10.1016/j.medmic.2025.100154","DOIUrl":"10.1016/j.medmic.2025.100154","url":null,"abstract":"<div><div>Alcoholic liver disease (ALD) remains a major global health burden driven by chronic alcohol consumption and characterized by progressive liver injury, inflammation, and fibrosis. A growing body of evidence highlights the central role of the gut-liver axis in ALD pathogenesis, where alcohol-induced dysbiosis and intestinal barrier disruption facilitate the translocation of bacterial endotoxins such as lipopolysaccharides (LPS) into the liver. These microbial products activate Kupffer cells via Toll-like receptor 4 (TLR4) signaling, triggering inflammatory cascades, oxidative stress, and hepatic stellate cell activation, thereby promoting fibrogenesis. Dysregulated bile acid metabolism, impaired FXR and TGR5 signaling, and depletion of beneficial microbial metabolites such as short-chain fatty acids (SCFAs) further contribute to liver damage. Advances in metabolomics have uncovered distinct microbial and host-derived metabolic signatures linked to disease severity, including SCFA depletion, elevated trimethylamine-N-oxide (TMAO), and bile acid imbalances. Precision interventions targeting the gut microbiota—such as probiotics, prebiotics, synbiotics, and microbial metabolite supplementation—are showing promise in modulating gut-liver interactions and mitigating ALD progression. Furthermore, the integration of multi-omics datasets with artificial intelligence (AI)-driven models is paving the way for personalized treatment strategies based on individual microbiome-metabolome profiles. This review consolidates current insights into ALD pathogenesis, the gut-liver axis, and emerging microbiota-centered precision therapies that are reshaping the future of ALD management.</div></div>","PeriodicalId":36019,"journal":{"name":"Medicine in Microecology","volume":"26 ","pages":"Article 100154"},"PeriodicalIF":0.0,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145361623","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}
Stunting remains a significant public health challenge, particularly in low- and middle-income countries, with long-term consequences for physical growth, cognitive development, and future economic productivity. Emerging evidence highlights the critical role of the gut microbiota in early life nutrition, immune development, and linear growth, offering new insights into the pathogenesis of stunting. Children with stunting often exhibit reduced microbial diversity, dysbiosis, and decreased production of beneficial metabolites such as short-chain fatty acids (SCFAs), which are essential for intestinal health and metabolic regulation. Probiotics, especially strains of Lactobacillus and Bifidobacterium, have shown promise in modulating gut microbiota composition, enhancing nutrient absorption, improving intestinal barrier function, and promoting growth outcomes in malnourished children. This review synthesizes the current evidence on the interplay between stunting, gut microbiota, and probiotic interventions, emphasizing their mechanistic links and therapeutic potential. We also discuss the challenges in implementing probiotics at scale, including strain-specific efficacy, variability in host responses, and the need for long-term clinical trials. Targeting the gut microbiota through probiotic supplementation may serve as a complementary strategy to conventional nutritional programs to prevent and mitigate childhood stunting.
{"title":"Gut microbiota dysbiosis and probiotic interventions in childhood stunting: Mechanistic insights and therapeutic potential","authors":"Rizqi Yanuar Pauzi , Annisa Nurul Ilmi , Laksita Widya Kumaratih","doi":"10.1016/j.medmic.2025.100152","DOIUrl":"10.1016/j.medmic.2025.100152","url":null,"abstract":"<div><div>Stunting remains a significant public health challenge, particularly in low- and middle-income countries, with long-term consequences for physical growth, cognitive development, and future economic productivity. Emerging evidence highlights the critical role of the gut microbiota in early life nutrition, immune development, and linear growth, offering new insights into the pathogenesis of stunting. Children with stunting often exhibit reduced microbial diversity, dysbiosis, and decreased production of beneficial metabolites such as short-chain fatty acids (SCFAs), which are essential for intestinal health and metabolic regulation. Probiotics, especially strains of Lactobacillus and Bifidobacterium, have shown promise in modulating gut microbiota composition, enhancing nutrient absorption, improving intestinal barrier function, and promoting growth outcomes in malnourished children. This review synthesizes the current evidence on the interplay between stunting, gut microbiota, and probiotic interventions, emphasizing their mechanistic links and therapeutic potential. We also discuss the challenges in implementing probiotics at scale, including strain-specific efficacy, variability in host responses, and the need for long-term clinical trials. Targeting the gut microbiota through probiotic supplementation may serve as a complementary strategy to conventional nutritional programs to prevent and mitigate childhood stunting.</div></div>","PeriodicalId":36019,"journal":{"name":"Medicine in Microecology","volume":"26 ","pages":"Article 100152"},"PeriodicalIF":0.0,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145226852","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 : 2025-09-13DOI: 10.1016/j.medmic.2025.100151
B. Aswinanand , Jeeva Balakrishnan , Kathiravan Muthu Kumaradoss , Mikhlid H. Almutairi , Bader O. Almutairi , S. Karthick Raja Namasivayam , Senthilkumar Palaniappan , Jesu Arockiaraj
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a growing health challenge worldwide, strongly connected to hyperglycemia (HG). This study investigates the therapeutic potential of 4-methyl-N-(6-methyl-1,3-benzothiazol-2-yl) benzene-1-sulfonamide (named KM9), a novel compound consisting of thiazol and sulfonyl groups, for HG-associated MASLD. In silico analysis using network pharmacology verified that KM9 is involved in lipid metabolism and insulin signaling pathways. In vitro and in vivo studies using HepG2 cells and zebrafish embryos demonstrated the cytotoxicity and effective dose of KM9. These studies further revealed its ability to reduce oxidative stress indicators, including reactive oxygen species (ROS), apoptosis, and lipid peroxidation (LPO) induced by alloxan (ALN). In ALN-exposed zebrafish, KM9 significantly reduced glucose levels and enhanced glucose uptake. It also lowered lipid accumulation, cholesterol, and triglyceride levels. KM9 exhibited anti-inflammatory effects by reducing macrophage localization and increased the activity of antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), and glutathione peroxidase (GPx). Furthermore, KM9 regulated genes associated with lipogenesis (fasn, srebp1), inflammation (il-6, tnf-α), and insulin receptor expression (ins, insra1, insrb1). These findings demonstrate that KM9 exerts multifaceted protective effects, which collectively decrease liver damage and improve liver health, as evidenced by histopathological analysis.
代谢功能障碍相关脂肪变性肝病（MASLD）是全球范围内日益增长的健康挑战，与高血糖（HG）密切相关。本研究研究了4-甲基- n -（6-甲基-1,3-苯并噻唑-2-基）苯-1-磺酰胺（命名为KM9），一种由噻唑和磺酰基组成的新型化合物，对hg相关MASLD的治疗潜力。网络药理学的计算机分析证实KM9参与脂质代谢和胰岛素信号通路。利用HepG2细胞和斑马鱼胚胎进行的体外和体内研究证实了KM9的细胞毒性和有效剂量。这些研究进一步揭示了其降低氧化应激指标的能力，包括活性氧（ROS）、细胞凋亡和四氧嘧啶（ALN）诱导的脂质过氧化（LPO）。在aln暴露的斑马鱼中，KM9显著降低了葡萄糖水平并增强了葡萄糖摄取。它还能降低脂质积累、胆固醇和甘油三酯水平。KM9通过降低巨噬细胞的定位和提高抗氧化酶的活性，包括超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽s -转移酶（GST）和谷胱甘肽过氧化物酶（GPx），具有抗炎作用。此外，KM9调节与脂肪生成（fasn, srebp1），炎症（il-6, tnf-α）和胰岛素受体表达（ins, insra1, insrb1）相关的基因。这些发现表明，KM9具有多方面的保护作用，其共同减少肝损伤和改善肝脏健康，正如组织病理学分析所证明的那样。
{"title":"Thiazol-sulfonyl derivative KM9 mitigates hyperglycemia-associated steatotic liver injury in in-vitro and in-vivo models","authors":"B. Aswinanand , Jeeva Balakrishnan , Kathiravan Muthu Kumaradoss , Mikhlid H. Almutairi , Bader O. Almutairi , S. Karthick Raja Namasivayam , Senthilkumar Palaniappan , Jesu Arockiaraj","doi":"10.1016/j.medmic.2025.100151","DOIUrl":"10.1016/j.medmic.2025.100151","url":null,"abstract":"<div><div>Metabolic dysfunction-associated steatotic liver disease (MASLD) is a growing health challenge worldwide, strongly connected to hyperglycemia (HG). This study investigates the therapeutic potential of 4-methyl-N-(6-methyl-1,3-benzothiazol-2-yl) benzene-1-sulfonamide (named KM9), a novel compound consisting of thiazol and sulfonyl groups, for HG-associated MASLD. In silico analysis using network pharmacology verified that KM9 is involved in lipid metabolism and insulin signaling pathways. In vitro and in vivo studies using HepG2 cells and zebrafish embryos demonstrated the cytotoxicity and effective dose of KM9. These studies further revealed its ability to reduce oxidative stress indicators, including reactive oxygen species (ROS), apoptosis, and lipid peroxidation (LPO) induced by alloxan (ALN). In ALN-exposed zebrafish, KM9 significantly reduced glucose levels and enhanced glucose uptake. It also lowered lipid accumulation, cholesterol, and triglyceride levels. KM9 exhibited anti-inflammatory effects by reducing macrophage localization and increased the activity of antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), and glutathione peroxidase (GPx). Furthermore, KM9 regulated genes associated with lipogenesis (<em>fasn</em>, <em>srebp1</em>), inflammation (<em>il-6</em>, <em>tnf-α</em>), and insulin receptor expression (<em>ins</em>, <em>insra1</em>, <em>insrb1</em>). These findings demonstrate that KM9 exerts multifaceted protective effects, which collectively decrease liver damage and improve liver health, as evidenced by histopathological analysis.</div></div>","PeriodicalId":36019,"journal":{"name":"Medicine in Microecology","volume":"26 ","pages":"Article 100151"},"PeriodicalIF":0.0,"publicationDate":"2025-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145105233","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}
The prevalence of antibiotic resistance has made ESKAPE pathogens a severe global health hazard, owing to the limits and regular failures of conventional treatment methods. The ESKAPE pathogens (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter species) are the most common causes of nosocomial diseases worldwide. Most of them are multidrug-resistant isolates, which pose one of the most significant difficulties in clinical treatment. The rising incidence of multidrug-resistant (MDR) advantageous infections in intensive care units (ICUs) is particularly concerning, as it poses a danger to public health and significantly impacts morbidity and death rates. MDR ESKAPE bacteria make up the great bulk of these opportunistic infections. Among these issues, nanotechnology appears as a potential area in the battle against biofilms. Considering their distinct characteristics at the nanoscale, provide novel antimicrobial techniques that are not present in standard defence mechanisms. Green-synthesized nanoparticles and their anti-biofilm qualities are highlighted in this in-depth examination of nanotechnology's possibility to combat biofilms. The prevalence of resistant microorganisms and antibiotics environmental residues need immediate worldwide encounter to avoid antimicrobial resistance (AMR). These natural medications may also be improved by adding silver nanoparticles and mixing them with current antibiotics. By focusing on ESKAPE organisms, the AMR problem may be tackled considerably more effectively.
{"title":"Nanotechnology targeting ESKAPE pathogens: Eco-friendly produced nanomaterials as an innovative antibiofilm approach","authors":"Arunagiri Ragu Prasath , Chinnasamy Ragavendran , Paramasivam Deepak , Nathiya Thiyagarajulu","doi":"10.1016/j.medmic.2025.100149","DOIUrl":"10.1016/j.medmic.2025.100149","url":null,"abstract":"<div><div>The prevalence of antibiotic resistance has made ESKAPE pathogens a severe global health hazard, owing to the limits and regular failures of conventional treatment methods. The ESKAPE pathogens (<em>Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa</em>, and <em>Enterobacter species</em>) are the most common causes of nosocomial diseases worldwide. Most of them are multidrug-resistant isolates, which pose one of the most significant difficulties in clinical treatment. The rising incidence of multidrug-resistant (MDR) advantageous infections in intensive care units (ICUs) is particularly concerning, as it poses a danger to public health and significantly impacts morbidity and death rates. MDR ESKAPE bacteria make up the great bulk of these opportunistic infections. Among these issues, nanotechnology appears as a potential area in the battle against biofilms. Considering their distinct characteristics at the nanoscale, provide novel antimicrobial techniques that are not present in standard defence mechanisms. Green-synthesized nanoparticles and their <em>anti</em>-biofilm qualities are highlighted in this in-depth examination of nanotechnology's possibility to combat biofilms. The prevalence of resistant microorganisms and antibiotics environmental residues need immediate worldwide encounter to avoid antimicrobial resistance (AMR). These natural medications may also be improved by adding silver nanoparticles and mixing them with current antibiotics. By focusing on ESKAPE organisms, the AMR problem may be tackled considerably more effectively.</div></div>","PeriodicalId":36019,"journal":{"name":"Medicine in Microecology","volume":"26 ","pages":"Article 100149"},"PeriodicalIF":0.0,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145019570","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}
The gut microbiota and immune system are significantly influenced by the human gut-virus axis, which is mostly composed of bacteriophages and eukaryotic viruses. Through mechanisms affecting microbial balance, immunological responses, and intestinal barrier integrity, recent research emphasizes its role in the onset and progression of inflammatory bowel disease (IBD). This review examines the ways in which gut viruses—bacteriophages in particular—contribute to dysbiosis through biofilm development, transduction, and bacterial diversity modulation. We also go over how the virome affects chronic inflammation and host immunological signaling. The virome in IBD patients can now be thoroughly profiled thanks to developments in metagenomic and viromic technologies, which have identified unique changes that could be used as therapeutic targets or diagnostic biomarkers. Integrating virome research into the larger framework of the gut microbiota offers a fresh viewpoint on the pathophysiology of IBD and has the potential to advance precision medicine techniques and virus-based treatments, despite the fact that the topic is still understudied.
{"title":"Gut virus axis: Unravelling viral contribution to gut microbiota dysbiosis and translational medicine in inflammatory bowel disease","authors":"Naziya Akhtar, Chirag Jain, Shikha Baghel Chauhan, Indu Singh","doi":"10.1016/j.medmic.2025.100148","DOIUrl":"10.1016/j.medmic.2025.100148","url":null,"abstract":"<div><div>The gut microbiota and immune system are significantly influenced by the human gut-virus axis, which is mostly composed of bacteriophages and eukaryotic viruses. Through mechanisms affecting microbial balance, immunological responses, and intestinal barrier integrity, recent research emphasizes its role in the onset and progression of inflammatory bowel disease (IBD). This review examines the ways in which gut viruses—bacteriophages in particular—contribute to dysbiosis through biofilm development, transduction, and bacterial diversity modulation. We also go over how the virome affects chronic inflammation and host immunological signaling. The virome in IBD patients can now be thoroughly profiled thanks to developments in metagenomic and viromic technologies, which have identified unique changes that could be used as therapeutic targets or diagnostic biomarkers. Integrating virome research into the larger framework of the gut microbiota offers a fresh viewpoint on the pathophysiology of IBD and has the potential to advance precision medicine techniques and virus-based treatments, despite the fact that the topic is still understudied.</div></div>","PeriodicalId":36019,"journal":{"name":"Medicine in Microecology","volume":"26 ","pages":"Article 100148"},"PeriodicalIF":0.0,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144925950","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 : 2025-08-23DOI: 10.1016/j.medmic.2025.100147
Michael Owen Hogipranata , Muhammad Reva Aditya , Imanuel Yuerrico Subianto , Virginie Trias Salim , Valeska Theodora Beatrice , Kana Mardhiyyah , Dewi Indiastari
Introduction
Human immunodeficiency virus (HIV) compromises the immune system by targeting key regulatory lymphocytes essential for coordinating immune responses. It continues to pose a significant global health burden, with approximately 40 million cases recorded by the end of 2023. Currently, highly active antiretroviral therapy (HAART) is the key therapeutic strategy, but it has several limitations, prompting the importance of new therapeutic approaches. This paper evaluates the effectiveness of gut microbiota basesd immunomodulatory therapies, consisting of prebiotics, probiotics, and synbiotics in HIV treatment while considering clinical, socioeconomic, and therapeutic influencing factors.
Methods
This study was conducted based on PRISMA guidelines using multiple databases. Studies were employed based on established inclusion parameters, focusing on the efficacy of gut microbiota interventions in CD4+ T-cell counts.Subgroup analyses were performed based on intervention type, dosage, duration, HAART status, and clinical setting. Moreover, sensitivity analysis, meta-regression, and publication bias assessment were also performed to ensure findings robustness and explore source of heterogeneity.
Results
A total of 21 studies were assessed in this meta-analysis. Risk of bias assessment indicated that most studies had a low risk of bias, though some concerns were noted. Prebiotics showed the greatest improvement by a mean difference (MD) of 52.15 cells/mm3 (95 % CI: −5.64 to 109.93), though not statistically significant (p = 0.08). Synbiotics showed a more consistent and statistically significant effect (MD = 39.48 cells/mm3; 95 % CI: 34.39 to 44.58; p < 0.00001). Notably, greatest immunological benefits were observed among HAART-naive individuals, with low-dose prebiotics (4–10 g/day), moderate intervention durations (4–6 months), and in low- and middle-income countries (LMICs). Sensitivity analysis using leave-one-out method confirmed findings robustness, while meta-regression identified key variables contributing to heterogeneity. Moreover, publication bias using Egger's and Begg's test was not evident in most outcomes, except for LMIC-based studies, which showed potential small-study effects.
Conclusion
Gut microbiota based immunomodulators show promising potential in supporting immune function among people living with HIV. However, due to study variability, high heterogeneity and wide confidence intervals (CI) in some subgroups, these findings are hypothesis-generating. Further high-quality studies should focused in homogeneous populations to validate efficacy and guide clinical implementation.
{"title":"Gut microbiota modulation using prebiotics, probiotics, and synbiotics for CD4+ T-cell recovery in HIV: A systematic review and meta-analysis","authors":"Michael Owen Hogipranata , Muhammad Reva Aditya , Imanuel Yuerrico Subianto , Virginie Trias Salim , Valeska Theodora Beatrice , Kana Mardhiyyah , Dewi Indiastari","doi":"10.1016/j.medmic.2025.100147","DOIUrl":"10.1016/j.medmic.2025.100147","url":null,"abstract":"<div><h3>Introduction</h3><div>Human immunodeficiency virus (HIV) compromises the immune system by targeting key regulatory lymphocytes essential for coordinating immune responses. It continues to pose a significant global health burden, with approximately 40 million cases recorded by the end of 2023. Currently, highly active antiretroviral therapy (HAART) is the key therapeutic strategy, but it has several limitations, prompting the importance of new therapeutic approaches. This paper evaluates the effectiveness of gut microbiota basesd immunomodulatory therapies, consisting of prebiotics, probiotics, and synbiotics in HIV treatment while considering clinical, socioeconomic, and therapeutic influencing factors.</div></div><div><h3>Methods</h3><div>This study was conducted based on PRISMA guidelines using multiple databases. Studies were employed based on established inclusion parameters, focusing on the efficacy of gut microbiota interventions in CD4<sup>+</sup> T-cell counts.Subgroup analyses were performed based on intervention type, dosage, duration, HAART status, and clinical setting. Moreover, sensitivity analysis, meta-regression, and publication bias assessment were also performed to ensure findings robustness and explore source of heterogeneity.</div></div><div><h3>Results</h3><div>A total of 21 studies were assessed in this meta-analysis. Risk of bias assessment indicated that most studies had a low risk of bias, though some concerns were noted. Prebiotics showed the greatest improvement by a mean difference (MD) of 52.15 cells/mm<sup>3</sup> (95 % CI: −5.64 to 109.93), though not statistically significant (p = 0.08). Synbiotics showed a more consistent and statistically significant effect (MD = 39.48 cells/mm<sup>3</sup>; 95 % CI: 34.39 to 44.58; p < 0.00001). Notably, greatest immunological benefits were observed among HAART-naive individuals, with low-dose prebiotics (4–10 g/day), moderate intervention durations (4–6 months), and in low- and middle-income countries (LMICs). Sensitivity analysis using leave-one-out method confirmed findings robustness, while meta-regression identified key variables contributing to heterogeneity. Moreover, publication bias using Egger's and Begg's test was not evident in most outcomes, except for LMIC-based studies, which showed potential small-study effects.</div></div><div><h3>Conclusion</h3><div>Gut microbiota based immunomodulators show promising potential in supporting immune function among people living with HIV. However, due to study variability, high heterogeneity and wide confidence intervals (CI) in some subgroups, these findings are hypothesis-generating. Further high-quality studies should focused in homogeneous populations to validate efficacy and guide clinical implementation.</div></div>","PeriodicalId":36019,"journal":{"name":"Medicine in Microecology","volume":"26 ","pages":"Article 100147"},"PeriodicalIF":0.0,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144925949","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 : 2025-08-20DOI: 10.1016/j.medmic.2025.100144
Balapuwaduge Isuru Layan Madusanka Mendis , L. Sarvananda , Thilini N. Jayasinghe , Iyanthimala Harshini Rajapakse , Arosha Sampath Dissanayake
The gut microbiota is a major component of the human microbiome, crucial for gastrointestinal function. Dysbiosis of the gut microbiota has been linked to the development, progression, and susceptibility to type 2 diabetes mellitus (T2DM) through energy and fatty acid metabolism, intestinal barrier integrity, glucose homeostasis, insulin sensitivity, and inflammatory pathways. Additional connections have been identified with obesity and the gut-brain axis. Key microbial metabolites include short-chain fatty acids (SCFAs), lipopolysaccharides, secondary bile acids (SBAs), branched-chain amino acids, tryptophan derivatives, trimethylamine N-oxide, imidazole propionate, bioactive peptides, postbiotics, and fasting-induced adipose factor. Individuals with T2DM often exhibit reduced microbial diversity, lower levels of SCFA-producing bacteria, and increased presence of opportunistic, endotoxin-producing gram-negative bacteria. Key microbial genera implicated in T2DM include Clostridium, Bifidobacterium, Akkermansia, Bacteroides, Lactobacillus spp., and members of the Firmicutes phylum. The gut microbiota is shaped by diet, medications, health conditions, genetics, lifestyle, and environmental factors. Despite the complex inter/intra-individual variability of the gut microbiome, robust evidence may emerge through large-scale cohort studies employing deep sequencing and metagenomics. This review provides novel insights into how gut microbiota-derived metabolites influence host physiology, epigenetics and gut-brain axis signaling using comprehensive synthesis of mechanisms, microbial mediators, synergistic factors, and therapeutic modulators in a single context, allowing readers to understand the holistic role of gut microbiota in T2DM pathophysiology. As T2DM is a complex metabolic disorder requiring multidimensional approaches, such integration offers valuable perspective for prevention and therapy. Emerging strategies, including fecal microbiota transplantation (FMT) and bacteriophage therapy, also show promise. A multidisciplinary research agenda, incorporating large-scale cohort studies, omics technologies, and systems biology, is essential to identify causal relationships and personalize interventions.
{"title":"Mechanisms and key mediators of gut microbiota and type 2 diabetes mellitus: A comprehensive overview","authors":"Balapuwaduge Isuru Layan Madusanka Mendis , L. Sarvananda , Thilini N. Jayasinghe , Iyanthimala Harshini Rajapakse , Arosha Sampath Dissanayake","doi":"10.1016/j.medmic.2025.100144","DOIUrl":"10.1016/j.medmic.2025.100144","url":null,"abstract":"<div><div>The gut microbiota is a major component of the human microbiome, crucial for gastrointestinal function. Dysbiosis of the gut microbiota has been linked to the development, progression, and susceptibility to type 2 diabetes mellitus (T2DM) through energy and fatty acid metabolism, intestinal barrier integrity, glucose homeostasis, insulin sensitivity, and inflammatory pathways. Additional connections have been identified with obesity and the gut-brain axis. Key microbial metabolites include short-chain fatty acids (SCFAs), lipopolysaccharides, secondary bile acids (SBAs), branched-chain amino acids, tryptophan derivatives, trimethylamine N-oxide, imidazole propionate, bioactive peptides, postbiotics, and fasting-induced adipose factor. Individuals with T2DM often exhibit reduced microbial diversity, lower levels of SCFA-producing bacteria, and increased presence of opportunistic, endotoxin-producing gram-negative bacteria. Key microbial genera implicated in T2DM include <em>Clostridium, Bifidobacterium, Akkermansia, Bacteroides, Lactobacillus</em> spp., and members of the <em>Firmicutes</em> phylum. The gut microbiota is shaped by diet, medications, health conditions, genetics, lifestyle, and environmental factors. Despite the complex inter/intra-individual variability of the gut microbiome, robust evidence may emerge through large-scale cohort studies employing deep sequencing and metagenomics. This review provides novel insights into how gut microbiota-derived metabolites influence host physiology, epigenetics and gut-brain axis signaling using comprehensive synthesis of mechanisms, microbial mediators, synergistic factors, and therapeutic modulators in a single context, allowing readers to understand the holistic role of gut microbiota in T2DM pathophysiology. As T2DM is a complex metabolic disorder requiring multidimensional approaches, such integration offers valuable perspective for prevention and therapy. Emerging strategies, including fecal microbiota transplantation (FMT) and bacteriophage therapy, also show promise. A multidisciplinary research agenda, incorporating large-scale cohort studies, omics technologies, and systems biology, is essential to identify causal relationships and personalize interventions.</div></div>","PeriodicalId":36019,"journal":{"name":"Medicine in Microecology","volume":"26 ","pages":"Article 100144"},"PeriodicalIF":0.0,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144920189","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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