Pub Date : 2024-12-09DOI: 10.1016/j.micres.2024.127986
Athanasios Nikolaou , Manuel Salvador , Ian Wright , Thomas Wantock , Gavin Sandison , Thomas Harle , Daniela Carta , Jorge Gutierrez-Merino
Reactive oxygen and nitrogen species (RONS) are emerging as a novel antibacterial strategy to combat the alarming increase in antimicrobial resistance (AMR). RONS can inhibit bacterial growth through reactions with cellular molecules, compromising vital biological functions and leading to cell death. While their mechanisms of action have been studied, many remain unclear, especially in biologically relevant environments. In this study, we exposed Gram-positive and Gram-negative bacteria to varying RONS ratios, mimicking what microbes may naturally encounter. A ratio in favour of RNS induced membrane depolarization and pore formation, resulting in an irreversible bactericidal effect. By contrast, ROS predominance caused membrane permeabilization and necrotic-like responses, leading to biofilm formation. Furthermore, bacterial cells exposed to more RNS than ROS activated metabolic processes associated with anaerobic respiration, DNA & cell wall/membrane repair, and cell signalling. Our findings suggest that the combination of ROS and RNS can be an effective alternative to inhibit bacteria, but only under higher RNS levels, as ROS dominance might foster bacterial tolerance, which in the context of AMR could have devastating consequences.
{"title":"The ratio of reactive oxygen and nitrogen species determines the type of cell death that bacteria undergo","authors":"Athanasios Nikolaou , Manuel Salvador , Ian Wright , Thomas Wantock , Gavin Sandison , Thomas Harle , Daniela Carta , Jorge Gutierrez-Merino","doi":"10.1016/j.micres.2024.127986","DOIUrl":"10.1016/j.micres.2024.127986","url":null,"abstract":"<div><div>Reactive oxygen and nitrogen species (RONS) are emerging as a novel antibacterial strategy to combat the alarming increase in antimicrobial resistance (AMR). RONS can inhibit bacterial growth through reactions with cellular molecules, compromising vital biological functions and leading to cell death. While their mechanisms of action have been studied, many remain unclear, especially in biologically relevant environments. In this study, we exposed Gram-positive and Gram-negative bacteria to varying RONS ratios, mimicking what microbes may naturally encounter. A ratio in favour of RNS induced membrane depolarization and pore formation, resulting in an irreversible bactericidal effect. By contrast, ROS predominance caused membrane permeabilization and necrotic-like responses, leading to biofilm formation. Furthermore, bacterial cells exposed to more RNS than ROS activated metabolic processes associated with anaerobic respiration, DNA & cell wall/membrane repair, and cell signalling. Our findings suggest that the combination of ROS and RNS can be an effective alternative to inhibit bacteria, but only under higher RNS levels, as ROS dominance might foster bacterial tolerance, which in the context of AMR could have devastating consequences.</div></div>","PeriodicalId":18564,"journal":{"name":"Microbiological research","volume":"292 ","pages":"Article 127986"},"PeriodicalIF":6.1,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142829325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Immunoglobulin A nephropathy (IgAN) is the most prevalent form of primary glomerulonephritis globally, yet its pathogenesis remains incompletely understood. While much research has focused on the gut microbiome in the development of the disease, emerging evidence suggests that the oropharyngeal microbiota may also be a potential contributor. Studies have revealed significant alterations in oropharyngeal microbial diversity and specific bacterial taxa in IgAN patients, correlating with disease severity and progression. This review aims to comprehensively summarize and discuss the key findings from in vitro, in vivo, and clinical studies into the oropharyngeal bacteria and microbiome alterations in IgAN. Clinical studies have identified associations between certain oropharyngeal bacteria, particularly Cnm+Streptococcus mutans, Campylobacter rectus, and Porphyromonas gingivalis with IgAN patients and severe clinical outcomes with. In vitro and in vivo studies further establish a causal relationship between IgAN and oropharyngeal bacteria such as Streptococcus and Haemophilus. Microbiome analyses demonstrate dysbiotic patterns in IgAN patients and identify new potential bacterial genera that have yet to be explored experimentally but may potentially contribute to the disease’s pathogenesis. Additionally, the use of these bacterial genera as diagnostic and prognostic biomarkers of IgAN has achieved promising performance. Overall, the evidence highlights the strong connection between oropharyngeal bacteria and IgAN through both causal and non-causal associations. Further investigation into these newly identified bacterial genera and integration of multi-omics data are necessary to uncover mechanisms, validate their role in IgAN, and potentially develop novel diagnostic and therapeutic approaches.
{"title":"Links between oropharyngeal microbiota and IgA nephropathy: A paradigm shift from isolated microbe to microbiome","authors":"Narongsak Tangon , Sirinart Kumfu , Nipon Chattipakorn , Siriporn C. Chattipakorn","doi":"10.1016/j.micres.2024.128005","DOIUrl":"10.1016/j.micres.2024.128005","url":null,"abstract":"<div><div>Immunoglobulin A nephropathy (IgAN) is the most prevalent form of primary glomerulonephritis globally, yet its pathogenesis remains incompletely understood. While much research has focused on the gut microbiome in the development of the disease, emerging evidence suggests that the oropharyngeal microbiota may also be a potential contributor. Studies have revealed significant alterations in oropharyngeal microbial diversity and specific bacterial taxa in IgAN patients, correlating with disease severity and progression. This review aims to comprehensively summarize and discuss the key findings from <em>in vitro</em>, <em>in vivo</em>, and clinical studies into the oropharyngeal bacteria and microbiome alterations in IgAN. Clinical studies have identified associations between certain oropharyngeal bacteria, particularly Cnm<sup>+</sup> <em>Streptococcus mutans</em>, <em>Campylobacter rectus</em>, and <em>Porphyromonas gingivalis</em> with IgAN patients and severe clinical outcomes with. <em>In vitro</em> and <em>in vivo</em> studies further establish a causal relationship between IgAN and oropharyngeal bacteria such as <em>Streptococcus</em> and <em>Haemophilus</em>. Microbiome analyses demonstrate dysbiotic patterns in IgAN patients and identify new potential bacterial genera that have yet to be explored experimentally but may potentially contribute to the disease’s pathogenesis. Additionally, the use of these bacterial genera as diagnostic and prognostic biomarkers of IgAN has achieved promising performance. Overall, the evidence highlights the strong connection between oropharyngeal bacteria and IgAN through both causal and non-causal associations. Further investigation into these newly identified bacterial genera and integration of multi-omics data are necessary to uncover mechanisms, validate their role in IgAN, and potentially develop novel diagnostic and therapeutic approaches.</div></div>","PeriodicalId":18564,"journal":{"name":"Microbiological research","volume":"292 ","pages":"Article 128005"},"PeriodicalIF":6.1,"publicationDate":"2024-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142829397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The emergence and rapid dissemination of carbapenem-resistant hypervirulent Klebsiella pneumoniae (CR-hvKP) pose a serious threat to public health. Antibiotic treatment failure of K. pneumoniae infections has been largely attributed to acquisition of antibiotic resistance and bacterial biofilm caused by the presence of antibiotic persisters. There is an urgent need for novel antimicrobial agents or therapy strategies to manage infections caused by these notorious pathogens. In this study, we screened a collection of compounds that can dissipate bacterial proton motive force (PMF) and intermediate metabolites that can suppress antibiotic tolerance, and identified an antifungal drug sulconazole which can act in combination with glucose or trehalose to exert strong antibacterial effect against starvation-induced CR-hvKP persisters. Investigation of underlying mechanisms showed that sulconazole alone caused dissipation of transmembrane PMF, and sulconazole used in combination with glucose or trehalose could significantly inhibit the efflux activity, reduce NADH and ATP levels, and cause intracellular accumulation of reactive oxygen species (ROS) in CR-hvKP persisters, eventually resulting in bacterial cell death. These findings suggest that the sulconazole and glucose/trehalose combination is highly effective in eradicating multidrug-resistant and hypervirulent K. pneumoniae persisters, and may be used in development of a feasible strategy for treatment of chronic and recurrent K. pneumoniae infections.
{"title":"Antimicrobial effect of sulconazole in combination with glucose/trehalose against carbapenem-resistant hypervirulent Klebsiella pneumoniae persisters","authors":"Miaomiao Xie , Kaichao Chen , Heng Heng , Edward Wai-Chi Chan , Sheng Chen","doi":"10.1016/j.micres.2024.128006","DOIUrl":"10.1016/j.micres.2024.128006","url":null,"abstract":"<div><div>The emergence and rapid dissemination of carbapenem-resistant hypervirulent <em>Klebsiella pneumoniae</em> (CR-hvKP) pose a serious threat to public health. Antibiotic treatment failure of <em>K. pneumoniae</em> infections has been largely attributed to acquisition of antibiotic resistance and bacterial biofilm caused by the presence of antibiotic persisters. There is an urgent need for novel antimicrobial agents or therapy strategies to manage infections caused by these notorious pathogens. In this study, we screened a collection of compounds that can dissipate bacterial proton motive force (PMF) and intermediate metabolites that can suppress antibiotic tolerance, and identified an antifungal drug sulconazole which can act in combination with glucose or trehalose to exert strong antibacterial effect against starvation-induced CR-hvKP persisters. Investigation of underlying mechanisms showed that sulconazole alone caused dissipation of transmembrane PMF, and sulconazole used in combination with glucose or trehalose could significantly inhibit the efflux activity, reduce NADH and ATP levels, and cause intracellular accumulation of reactive oxygen species (ROS) in CR-hvKP persisters, eventually resulting in bacterial cell death. These findings suggest that the sulconazole and glucose/trehalose combination is highly effective in eradicating multidrug-resistant and hypervirulent <em>K. pneumoniae</em> persisters, and may be used in development of a feasible strategy for treatment of chronic and recurrent <em>K. pneumoniae</em> infections.</div></div>","PeriodicalId":18564,"journal":{"name":"Microbiological research","volume":"292 ","pages":"Article 128006"},"PeriodicalIF":6.1,"publicationDate":"2024-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142822099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A detailed diversity analysis of the prokaryotic and fungal communities in soil impacted by an underground fire located in the Trans-Mexican volcanic belt, Mexico, is described. Microbial diversity data obtained from soils at different depths and temperatures (27 °C, 42 °C, 50 ºC and 54 ºC) were analyzed, and Firmicutes increased in abundance as the temperature augmented, and Proteobacteria mainly decreased in abundance at high temperatures compared to unaffected soils. The fungal phylum Ascomycota was the most abundant, with no significant changes. A clear reduction in the richness of both prokaryotic and eukaryotic operational taxonomic units (OTUs) was observed in the affected soils. At the genus level, Bacillus species were the most abundant among bacteria, while Aspergillus, Penicillium, and Mortierella were dominant fungal genera at higher temperatures. Interestingly, the physicochemical parameters of the affected soils modified organic matter, which was indirectly correlated with the presence of some microbial taxa. Likewise, we obtained 308 soil bacterial isolates from both control and affected soils. Among these, the taxa from the phyla Actinobacteria and Firmicutes demonstrated the highest thermotolerance in the affected soils. Our findings shed light on the impact of underground fires on the structure of microbial communities, favoring an abundance of thermotolerant microbes.
{"title":"Underground fires shape the structure of microbial communities and select for thermophilic bacteria through a temperature gradient","authors":"Aurora Flores-Piña, Eduardo Valencia-Cantero, Gustavo Santoyo","doi":"10.1016/j.micres.2024.127996","DOIUrl":"10.1016/j.micres.2024.127996","url":null,"abstract":"<div><div>A detailed diversity analysis of the prokaryotic and fungal communities in soil impacted by an underground fire located in the Trans-Mexican volcanic belt, Mexico, is described. Microbial diversity data obtained from soils at different depths and temperatures (27 °C, 42 °C, 50 ºC and 54 ºC) were analyzed, and Firmicutes increased in abundance as the temperature augmented, and Proteobacteria mainly decreased in abundance at high temperatures compared to unaffected soils. The fungal phylum Ascomycota was the most abundant, with no significant changes. A clear reduction in the richness of both prokaryotic and eukaryotic operational taxonomic units (OTUs) was observed in the affected soils. At the genus level, <em>Bacillus</em> species were the most abundant among bacteria, while <em>Aspergillus</em>, <em>Penicillium</em>, and <em>Mortierella</em> were dominant fungal genera at higher temperatures. Interestingly, the physicochemical parameters of the affected soils modified organic matter, which was indirectly correlated with the presence of some microbial taxa. Likewise, we obtained 308 soil bacterial isolates from both control and affected soils. Among these, the taxa from the phyla Actinobacteria and Firmicutes demonstrated the highest thermotolerance in the affected soils. Our findings shed light on the impact of underground fires on the structure of microbial communities, favoring an abundance of thermotolerant microbes.</div></div>","PeriodicalId":18564,"journal":{"name":"Microbiological research","volume":"292 ","pages":"Article 127996"},"PeriodicalIF":6.1,"publicationDate":"2024-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142822101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-06DOI: 10.1016/j.micres.2024.127995
Shuxun Liu , Xujie Feng , Hangjia Zhang , Ping Li , Baoru Yang , Qing Gu
This review provides a comprehensive analysis of the intricate architecture of bacterial sensing systems, with a focus on signal transduction mechanisms and their critical roles in microbial physiology. It highlights quorum sensing (QS), quorum quenching (QQ), and quorum sensing interference (QSI) as fundamental processes driving bacterial communication, influencing gene expression, biofilm formation, and interspecies interactions. The analysis explores the importance of diffusible signal factors (DSFs) and secondary messengers such as cAMP and c-di-GMP in modulating microbial behaviors. Additionally, cross-kingdom signaling, where bacterial signals impact host-pathogen dynamics and ecological balance, is systematically reviewed. This review introduces “signalomics”, an novel interdisciplinary framework integrating genomics, proteomics, and metabolomics to offer a holistic framework for understanding microbial communication and evolution. These findings hold significant implications for various domains, including food preservation, agriculture, and human health.
{"title":"Decoding bacterial communication: Intracellular signal transduction, quorum sensing, and cross-kingdom interactions","authors":"Shuxun Liu , Xujie Feng , Hangjia Zhang , Ping Li , Baoru Yang , Qing Gu","doi":"10.1016/j.micres.2024.127995","DOIUrl":"10.1016/j.micres.2024.127995","url":null,"abstract":"<div><div>This review provides a comprehensive analysis of the intricate architecture of bacterial sensing systems, with a focus on signal transduction mechanisms and their critical roles in microbial physiology. It highlights quorum sensing (QS), quorum quenching (QQ), and quorum sensing interference (QSI) as fundamental processes driving bacterial communication, influencing gene expression, biofilm formation, and interspecies interactions. The analysis explores the importance of diffusible signal factors (DSFs) and secondary messengers such as cAMP and c-di-GMP in modulating microbial behaviors. Additionally, cross-kingdom signaling, where bacterial signals impact host-pathogen dynamics and ecological balance, is systematically reviewed. This review introduces “signalomics”, an novel interdisciplinary framework integrating genomics, proteomics, and metabolomics to offer a holistic framework for understanding microbial communication and evolution. These findings hold significant implications for various domains, including food preservation, agriculture, and human health.</div></div>","PeriodicalId":18564,"journal":{"name":"Microbiological research","volume":"292 ","pages":"Article 127995"},"PeriodicalIF":6.1,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142807159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-06DOI: 10.1016/j.micres.2024.127985
Zhiqiang Li , Xiao Yang , Yuxin Guo , Xiaofeng Zhang , You Li , Yen-Wen Kuo , Taiyun Wei , Qian Chen
The citrus disease Huanglongbing (HLB) in Asia and the US is caused by Candidatus Liberibacter asiaticus (CLas), which is primarily transmitted by Diaphorina citri, also known as Asian citrus psyllid in a persistent and propagative manner. However, the exact mechanisms underlying CLas circulation within D. citri remain largely unclear. Here, immunofluorescence microscopy and electron microscopy were utilized to track the sequential infection of CLas in D. citri, from alimentary canal to salivary glands, and ultimately to the plant host. CLas was found to initially infect the epithelium of filter chamber, after which it rapidly spreads to visceral muscles for further infection throughout the alimentary canal. The rapid spread in D. citri adults causes the duration of CLas circulation to be as short as 9 days. The duration of latent period may be explained by the recruitment of cytoskeletal α-actinin by the outer membrane protein (OMP) of CLas. Inhibition of actin filament or knocking down the expression of α-actinin significantly suppresses CLas cytoskeleton-dependent infection in and spread among D. citri organs. Injection of prokaryotically expressed OMP into D. citri also recruits α-actinin, resembling the natural infection of CLas. Our studies showed that CLas exploits α-actinin and remolds actin machinery of D. citri for overcoming the midgut release barrier, facilitating its circulation in the vector. By shedding light on these mechanisms, this report reveals more detailed mechanisms in CLas infection in D. citri, and offers a plausible explanation for rapid dissemination of HLB in nature from the perspective of psyllid transmission.
{"title":"Candidatus Liberibacter asiaticus exploits cytoskeletal system of psyllid vector for circulative propagative infection","authors":"Zhiqiang Li , Xiao Yang , Yuxin Guo , Xiaofeng Zhang , You Li , Yen-Wen Kuo , Taiyun Wei , Qian Chen","doi":"10.1016/j.micres.2024.127985","DOIUrl":"10.1016/j.micres.2024.127985","url":null,"abstract":"<div><div>The citrus disease Huanglongbing (HLB) in Asia and the US is caused by <em>Candidatus</em> Liberibacter asiaticus (<em>C</em>Las), which is primarily transmitted by <em>Diaphorina citri</em>, also known as Asian citrus psyllid in a persistent and propagative manner. However, the exact mechanisms underlying <em>C</em>Las circulation within <em>D. citri</em> remain largely unclear. Here, immunofluorescence microscopy and electron microscopy were utilized to track the sequential infection of <em>C</em>Las in <em>D. citri</em>, from alimentary canal to salivary glands, and ultimately to the plant host. <em>C</em>Las was found to initially infect the epithelium of filter chamber, after which it rapidly spreads to visceral muscles for further infection throughout the alimentary canal. The rapid spread in <em>D. citri</em> adults causes the duration of <em>C</em>Las circulation to be as short as 9 days. The duration of latent period may be explained by the recruitment of cytoskeletal α-actinin by the outer membrane protein (OMP) of <em>C</em>Las. Inhibition of actin filament or knocking down the expression of <em>α-actinin</em> significantly suppresses <em>C</em>Las cytoskeleton-dependent infection in and spread among <em>D. citri</em> organs. Injection of prokaryotically expressed OMP into <em>D. citri</em> also recruits α-actinin, resembling the natural infection of <em>C</em>Las. Our studies showed that <em>C</em>Las exploits α-actinin and remolds actin machinery of <em>D. citri</em> for overcoming the midgut release barrier, facilitating its circulation in the vector. By shedding light on these mechanisms, this report reveals more detailed mechanisms in <em>C</em>Las infection in <em>D. citri</em>, and offers a plausible explanation for rapid dissemination of HLB in nature from the perspective of psyllid transmission.</div></div>","PeriodicalId":18564,"journal":{"name":"Microbiological research","volume":"292 ","pages":"Article 127985"},"PeriodicalIF":6.1,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142823836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-30DOI: 10.1016/j.micres.2024.127987
Beiliang Miao , Dianhong Wang , Li Yu , Xiangfei Meng , Shiyi Liu , Mengqi Gao , Jiatong Han , Zeliang Chen , Ping Li , Shiwei Liu
Bacterial biofilms are one of the most relevant drivers of chronic and recurrent infections and a significant healthcare problem. Biofilms were formed by cross-linking of hydrophobic extracellular polymeric substances (EPS), such as proteins, polysaccharides, and eDNA, which were synthesized by bacteria themselves after adhesion and colonization on biological surfaces. They had the characteristics of dense structure and low drug permeability, leading to tolerance and resistance of biofilms to antibiotics and to host responses. Within a biofilm, microbial cells show increased tolerance to both immune system defense mechanisms and antimicrobials than the same cells in the planktonic state. It is one of the key reasons for the failure of traditional clinical drug to treat infectious diseases. Currently, no drugs are available to attack bacterial biofilms in the clinical setting. The development of novel preventive and therapeutic strategies is urgently needed to allow an effective management of biofilm-associated infections. Based on the properties of nanomaterials and biocompatibility, nanotechnology had the advantages of specific targeting, intelligent delivery and low toxicity, which could realize efficient intervention and precise treatment of biofilm-associated infections. In this paper, the mechanisms of bacterial biofilm resistance to antibiotics and host response tolerance were elaborated. Meanwhile, This paper highlighted multiple strategies of biofilms eradication based on nanotechnology. Nanotechnology can interfere with biofilm formation by destroying mature biofilm, modulating biofilm heterogeneity, inhibiting bacterial metabolism, playing antimicrobial properties, activating immunity and enhancing biofilm penetration, which is an important new anti-biofilm preparation. In addition, we presented the key challenges still faced by nanotechnology in combating bacterial biofilm infections. Utilization of nanotechnology safely and effectively should be further strengthened to confirm the safety aspects of their clinical application.
{"title":"Mechanism and nanotechnological-based therapeutics for tolerance and resistance of bacterial biofilms","authors":"Beiliang Miao , Dianhong Wang , Li Yu , Xiangfei Meng , Shiyi Liu , Mengqi Gao , Jiatong Han , Zeliang Chen , Ping Li , Shiwei Liu","doi":"10.1016/j.micres.2024.127987","DOIUrl":"10.1016/j.micres.2024.127987","url":null,"abstract":"<div><div>Bacterial biofilms are one of the most relevant drivers of chronic and recurrent infections and a significant healthcare problem. Biofilms were formed by cross-linking of hydrophobic extracellular polymeric substances (EPS), such as proteins, polysaccharides, and eDNA, which were synthesized by bacteria themselves after adhesion and colonization on biological surfaces. They had the characteristics of dense structure and low drug permeability, leading to tolerance and resistance of biofilms to antibiotics and to host responses. Within a biofilm, microbial cells show increased tolerance to both immune system defense mechanisms and antimicrobials than the same cells in the planktonic state. It is one of the key reasons for the failure of traditional clinical drug to treat infectious diseases. Currently, no drugs are available to attack bacterial biofilms in the clinical setting. The development of novel preventive and therapeutic strategies is urgently needed to allow an effective management of biofilm-associated infections. Based on the properties of nanomaterials and biocompatibility, nanotechnology had the advantages of specific targeting, intelligent delivery and low toxicity, which could realize efficient intervention and precise treatment of biofilm-associated infections. In this paper, the mechanisms of bacterial biofilm resistance to antibiotics and host response tolerance were elaborated. Meanwhile, This paper highlighted multiple strategies of biofilms eradication based on nanotechnology. Nanotechnology can interfere with biofilm formation by destroying mature biofilm, modulating biofilm heterogeneity, inhibiting bacterial metabolism, playing antimicrobial properties, activating immunity and enhancing biofilm penetration, which is an important new anti-biofilm preparation. In addition, we presented the key challenges still faced by nanotechnology in combating bacterial biofilm infections. Utilization of nanotechnology safely and effectively should be further strengthened to confirm the safety aspects of their clinical application.</div></div>","PeriodicalId":18564,"journal":{"name":"Microbiological research","volume":"292 ","pages":"Article 127987"},"PeriodicalIF":6.1,"publicationDate":"2024-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-29DOI: 10.1016/j.micres.2024.127979
Jie Zhang, Panlei Yang, Qingchao Zeng, Yiwei Zhang, Yanan Zhao, Liwei Wang, Yan Li, Zhenshuo Wang, Qi Wang
Robust biofilm formation on host niches facilitates beneficial Bacillus to promote plant growth and inhibit plant pathogens. Arginine kinase McsB is involved in bacterial development and stress reaction by phosphorylating proteins for degradation through a ClpC/ClpP protease. Conversely, cognate arginine phosphatase YwlE counteracts the process. Regulatory pathways of biofilm formation have been studied in Bacillus subtilis, of which Spo0A∼P is a master transcriptional regulator, which is transcriptionally activated by itself in biofilm formation. Previous studies have shown that Spo0A∼P transcript regulation controls biofilm formation, where MecA binds ClpC to inhibit Spo0A∼P-dependent transcription without triggering degradation. It remains unclear whether McsB and ClpC regulate biofilm formation together and share a similar non-proteolytic mechanism like MecA/ClpC complex. In this study, we characterized McsB and ClpC as negative regulators of biofilm formation and matrix gene eps expression. Our genetic and morphological evidence further indicates that McsB and ClpC inhibit eps expression by decreasing the spo0A and sinI expression, leading to the release of SinR, a known repressor of eps transcription. Given that the spo0A and sinI expression is transcriptionally activated by Spo0A∼P in biofilm formation, we next demonstrate that McsB interacts with Spo0A directly by bacterial two-hybrid system and Glutathione transferase pull-down experiments. Additionally, we present that McsB forms a complex with ClpC to dampen biofilm formation in vivo. Finally, we show that YwlE acts as a positive regulator of biofilm formation, counteracting the function of McsB. These findings suggest that McsB, ClpC, and YwlE play vital roles in the transition to biofilm formation in Bacillus subtilis, providing new insights into the regulatory mechanisms underlying biofilm development and sharing a similar non-proteolytic mechanism in biofilm formation as MecA/ClpC complex.
{"title":"Arginine kinase McsB and ClpC complex impairs the transition to biofilm formation in Bacillus subtilis","authors":"Jie Zhang, Panlei Yang, Qingchao Zeng, Yiwei Zhang, Yanan Zhao, Liwei Wang, Yan Li, Zhenshuo Wang, Qi Wang","doi":"10.1016/j.micres.2024.127979","DOIUrl":"10.1016/j.micres.2024.127979","url":null,"abstract":"<div><div>Robust biofilm formation on host niches facilitates beneficial <em>Bacillus</em> to promote plant growth and inhibit plant pathogens. Arginine kinase McsB is involved in bacterial development and stress reaction by phosphorylating proteins for degradation through a ClpC/ClpP protease. Conversely, cognate arginine phosphatase YwlE counteracts the process. Regulatory pathways of biofilm formation have been studied in <em>Bacillus subtilis</em>, of which Spo0A∼P is a master transcriptional regulator, which is transcriptionally activated by itself in biofilm formation. Previous studies have shown that Spo0A∼P transcript regulation controls biofilm formation, where MecA binds ClpC to inhibit Spo0A∼P-dependent transcription without triggering degradation. It remains unclear whether McsB and ClpC regulate biofilm formation together and share a similar non-proteolytic mechanism like MecA/ClpC complex. In this study, we characterized McsB and ClpC as negative regulators of biofilm formation and matrix gene <em>eps</em> expression. Our genetic and morphological evidence further indicates that McsB and ClpC inhibit <em>eps</em> expression by decreasing the <em>spo0A</em> and <em>sinI</em> expression, leading to the release of SinR, a known repressor of <em>eps</em> transcription. Given that the <em>spo0A</em> and <em>sinI</em> expression is transcriptionally activated by Spo0A∼P in biofilm formation, we next demonstrate that McsB interacts with Spo0A directly by bacterial two-hybrid system and Glutathione transferase pull-down experiments. Additionally, we present that McsB forms a complex with ClpC to dampen biofilm formation <em>in vivo</em>. Finally, we show that YwlE acts as a positive regulator of biofilm formation, counteracting the function of McsB. These findings suggest that McsB, ClpC, and YwlE play vital roles in the transition to biofilm formation in <em>Bacillus subtilis</em>, providing new insights into the regulatory mechanisms underlying biofilm development and sharing a similar non-proteolytic mechanism in biofilm formation as MecA/ClpC complex.</div></div>","PeriodicalId":18564,"journal":{"name":"Microbiological research","volume":"292 ","pages":"Article 127979"},"PeriodicalIF":6.1,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142823835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Phytoplasmas are phloem-limited plant pathogenic bacteria causing diseases in many plant species. They are transmitted by Hemipteran insect species in a persistent-propagative manner. Phytoplasmas are wall-less, and their membrane proteins are involved in pathogen internalization into host cells. We focused on the immunodominant membrane protein (Imp) of Flavescence dorée phytoplasma (FDp), a grapevine quarantine pest and a major threat to European viticulture. Scaphoideus titanus is the main natural vector of FDp to grapevine, whereas Euscelidius variegatus is commonly used as laboratory vector. Previous works indicated that recombinant Imp of two FDp strains (FD-C and FD-D) selectively interact with gut proteins from vector species rather than those from non-vectors. Here, similar patterns of interacting insect gut proteins were obtained from both vector species, following pull-down with His-tagged FDp Imps. After identification of several targets, four S. titanus and five E. variegatus proteins interacting with Imp were further characterized by measuring expression in different insect tissues and in healthy vs. infected insects. Specific RNAi silencing of two of these vector genes, namely natterin and legumain, resulted in a significant reduction of phytoplasma multiplication in insects upon pathogen acquisition, compared to control insects. Natterin displays a DM9 domain and legumain possesses a signature of G protein receptor, supporting their involvement as FDp Imp receptors. Outcomes of this work are discussed with particular attention devoted to the gain of knowledge on host/pathogen interaction as well as to the potential impact on improvement phytoplasma disease management.
{"title":"Natterin-like and legumain insect gut proteins promote the multiplication of a vector-borne bacterial plant pathogen","authors":"Luciana Galetto , Giulia Lucetti , Luca Bucci , Francesca Canuto , Marika Rossi , Simona Abbà , Marta Vallino , Cecilia Parise , Sabrina Palmano , Marcello Manfredi , Domenico Bosco , Cristina Marzachì","doi":"10.1016/j.micres.2024.127984","DOIUrl":"10.1016/j.micres.2024.127984","url":null,"abstract":"<div><div>Phytoplasmas are phloem-limited plant pathogenic bacteria causing diseases in many plant species. They are transmitted by Hemipteran insect species in a persistent-propagative manner. Phytoplasmas are wall-less, and their membrane proteins are involved in pathogen internalization into host cells. We focused on the immunodominant membrane protein (Imp) of Flavescence dorée phytoplasma (FDp), a grapevine quarantine pest and a major threat to European viticulture. <em>Scaphoideus titanus</em> is the main natural vector of FDp to grapevine, whereas <em>Euscelidius variegatus</em> is commonly used as laboratory vector. Previous works indicated that recombinant Imp of two FDp strains (FD-C and FD-D) selectively interact with gut proteins from vector species rather than those from non-vectors. Here, similar patterns of interacting insect gut proteins were obtained from both vector species, following pull-down with His-tagged FDp Imps. After identification of several targets, four <em>S. titanus</em> and five <em>E. variegatus</em> proteins interacting with Imp were further characterized by measuring expression in different insect tissues and in healthy vs. infected insects. Specific RNAi silencing of two of these vector genes, namely natterin and legumain, resulted in a significant reduction of phytoplasma multiplication in insects upon pathogen acquisition, compared to control insects. Natterin displays a DM9 domain and legumain possesses a signature of G protein receptor, supporting their involvement as FDp Imp receptors. Outcomes of this work are discussed with particular attention devoted to the gain of knowledge on host/pathogen interaction as well as to the potential impact on improvement phytoplasma disease management.</div></div>","PeriodicalId":18564,"journal":{"name":"Microbiological research","volume":"291 ","pages":"Article 127984"},"PeriodicalIF":6.1,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142757750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-28DOI: 10.1016/j.micres.2024.127967
Shang-Yu Li , Chenliu He , Cesar Augusto Valades-Cruz , Cheng-Cai Zhang , Yiling Yang
Light-controlled motility is advantageous for photosynthetic prokaryotes to better survive in environment with constantly changing light conditions. For cyanobacteria, light is both an energy source for photosynthesis and a stress factor. Consequently, some cyanobacteria evolved the ability to control type-IV pili (T4P)-mediated surface motility using a chemotaxis-like system in response to light signals. Extensive studies on the mechanism of phototaxis has been conducted in the spherical Synechocystis sp. PCC 6803 and the filamentous strain Nostoc punctiforme, while less is explored in rod-shaped cyanobacteria such as Synechococcus species. In this study, we investigated the phototaxis pathway in the unicellular rod-shaped cyanobacterium Synechococcus elongatus UTEX 3055, which exhibits bidirectional phototaxis using a single tax1 operon, in contrast to more complex and multiple gene clusters revealed in Synechocystis sp. PCC 6803. Results obtained by protein-protein interaction assays and protein subcellular localization experiments indicated that proteins encoded by the tax1 operon form large clusters that asymmetrically distributed both between the two poles and within the same pole. In vitro phosphorylation assays and site-directed mutations of conserved phosphorylation sites in PixLSe, PixGSe and PixHSe demonstrate that PixLSe acts as a histidine kinase, and PixGSe and PixHSe as response regulators for signal transduction. We further show that PixGSe and PixHSe are recruited to cell poles via interactions with the N-terminal region of PixLSe. While phosphotransfer reactions in this signaling pathway are critical for phototactic signaling, the two response regulators appear to play different roles in the control of phototaxis. This study provides a framework for further investigation into the complex phototactic signaling network in rod-shaped cyanobacteria with clearly defined cell poles in contrast to round shaped Synechocystis species with virtual cells poles through light-lensing effect.
{"title":"Phototactic signaling network in rod-shaped cyanobacteria: A study on Synechococcus elongatus UTEX 3055","authors":"Shang-Yu Li , Chenliu He , Cesar Augusto Valades-Cruz , Cheng-Cai Zhang , Yiling Yang","doi":"10.1016/j.micres.2024.127967","DOIUrl":"10.1016/j.micres.2024.127967","url":null,"abstract":"<div><div>Light-controlled motility is advantageous for photosynthetic prokaryotes to better survive in environment with constantly changing light conditions. For cyanobacteria, light is both an energy source for photosynthesis and a stress factor. Consequently, some cyanobacteria evolved the ability to control type-IV pili (T4P)-mediated surface motility using a chemotaxis-like system in response to light signals. Extensive studies on the mechanism of phototaxis has been conducted in the spherical <em>Synechocystis</em> sp. PCC 6803 and the filamentous strain <em>Nostoc punctiforme</em>, while less is explored in rod-shaped cyanobacteria such as <em>Synechococcus</em> species. In this study, we investigated the phototaxis pathway in the unicellular rod-shaped cyanobacterium <em>Synechococcus elongatus</em> UTEX 3055, which exhibits bidirectional phototaxis using a single <em>tax1</em> operon, in contrast to more complex and multiple gene clusters revealed in <em>Synechocystis</em> sp. PCC 6803. Results obtained by protein-protein interaction assays and protein subcellular localization experiments indicated that proteins encoded by the <em>tax1</em> operon form large clusters that asymmetrically distributed both between the two poles and within the same pole. <em>In vitro</em> phosphorylation assays and site-directed mutations of conserved phosphorylation sites in PixL<sub>Se</sub>, PixG<sub>Se</sub> and PixH<sub>Se</sub> demonstrate that PixL<sub>Se</sub> acts as a histidine kinase, and PixG<sub>Se</sub> and PixH<sub>Se</sub> as response regulators for signal transduction. We further show that PixG<sub>Se</sub> and PixH<sub>Se</sub> are recruited to cell poles via interactions with the N-terminal region of PixL<sub>Se</sub>. While phosphotransfer reactions in this signaling pathway are critical for phototactic signaling, the two response regulators appear to play different roles in the control of phototaxis. This study provides a framework for further investigation into the complex phototactic signaling network in rod-shaped cyanobacteria with clearly defined cell poles in contrast to round shaped <em>Synechocystis</em> species with virtual cells poles through light-lensing effect.</div></div>","PeriodicalId":18564,"journal":{"name":"Microbiological research","volume":"292 ","pages":"Article 127967"},"PeriodicalIF":6.1,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142786085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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