Antibiotic-resistant pathogens in public settings present a growing risk to human health. Staphylococcus aureus often asymptomatically colonizes human skin, while virulent strains cause soft tissue infections, osteomyelitis, endocarditis, and are associated with cystic fibrosis. Here we investigated the presence and distribution of multidrug-resistant S. aureus on exercise equipment in university recreation facilities. Equipment sampled included barbells (n = 10), dumbbell handles (n = 15), kettle bell handles (n = 5), ellipticals (n = 5), treadmills (n = 5), cable attachments (n = 5). Mannitol salt agar, CHROMagar-MRSA, Gram staining and latex agglutination testing were useds to isolate and identify S. aureus, including methicillin-resistant S. aureus. Kirby-Bauer disc-diffusion assay was utilized to determine antibiotic susceptibility profiles. Results show 42% of 456 S. aureus isolates from 45 different equipment surfaces were ampicillin resistant. Of 60 representative ampicillin-resistant isolates, 92% were resistant to additional antibiotics with the majority resistant to erythromycin (40%) and sulfisoxazole (75%). Multidrug resistance to three or more drugs was observed in 73% of the ampicillin-resistant subpopulation. These results indicate recreational facilities may serve as reservoirs for multi-drug resistant S. aureus including methicillin-resistant S. aureus (MRSA) and regular disinfection of equipment is warranted for safeguarding public health.
{"title":"Recreational Facilities as Reservoirs for Multidrug-Resistant Staphylococcus aureus","authors":"Chase A. Weikel, John M. Pisciotta","doi":"10.1111/1348-0421.13197","DOIUrl":"10.1111/1348-0421.13197","url":null,"abstract":"<div>\u0000 \u0000 <p>Antibiotic-resistant pathogens in public settings present a growing risk to human health. <i>Staphylococcus aureus</i> often asymptomatically colonizes human skin, while virulent strains cause soft tissue infections, osteomyelitis, endocarditis, and are associated with cystic fibrosis. Here we investigated the presence and distribution of multidrug-resistant <i>S. aureus</i> on exercise equipment in university recreation facilities. Equipment sampled included barbells (<i>n</i> = 10), dumbbell handles (<i>n</i> = 15), kettle bell handles (<i>n</i> = 5), ellipticals (<i>n</i> = 5), treadmills (<i>n</i> = 5), cable attachments (<i>n</i> = 5). Mannitol salt agar, CHROMagar-MRSA, Gram staining and latex agglutination testing were useds to isolate and identify <i>S. aureus</i>, including methicillin-resistant <i>S. aureus</i>. Kirby-Bauer disc-diffusion assay was utilized to determine antibiotic susceptibility profiles. Results show 42% of 456 <i>S. aureus</i> isolates from 45 different equipment surfaces were ampicillin resistant. Of 60 representative ampicillin-resistant isolates, 92% were resistant to additional antibiotics with the majority resistant to erythromycin (40%) and sulfisoxazole (75%). Multidrug resistance to three or more drugs was observed in 73% of the ampicillin-resistant subpopulation. These results indicate recreational facilities may serve as reservoirs for multi-drug resistant <i>S. aureus</i> including methicillin-resistant <i>S. aureus</i> (MRSA) and regular disinfection of equipment is warranted for safeguarding public health.</p>\u0000 </div>","PeriodicalId":18679,"journal":{"name":"Microbiology and Immunology","volume":"69 3","pages":"168-173"},"PeriodicalIF":1.9,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142882541","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The oral microbiome is closely involved in the maintenance of host health and the development of systemic diseases. The salivary glands play an essential role in homeostasis in the oral cavity. Here, we investigated the effects of periodontal inflammation on salivary gland function and the oral microbiome. In experimental periodontitis model mice, an increase in IgA⁺ cells in the salivary glands were observed 1 week after treatment. Alteration of the oral microbiome was also induced in this model. Gene expression analysis of the salivary glands showed changes in the expression of genes related to B-cell maturation and plasma cell differentiation and an increase in the expression of genes related to macrophage activation upon experimental periodontitis induction. Furthermore, the relationship between disruption of oral microflora and salivary gland function was examined using a cohousing model in which experimental periodontitis model mice and untreated mice were reared in the same cage. We found that cohoused normal mice underwent alteration of the oral microbiome, with increases in IgA⁺ cells and macrophages in the salivary glands. In summary, our results suggest that, in the oral cavity, there is a close link between oral bacterial flora and immune cells in the salivary glands. Our results also show that localized inflammation disrupts the homeostasis in the oral cavity, inducing pathological conditions such as dysbiosis. Our study suggests the importance of the interaction among local oral inflammation, salivary gland function, and oral microflora, and provides new insights into the mechanisms by which oral health is maintained.
{"title":"Experimental Murine Periodontitis Increases Salivary Gland IgA-Producing B Cells Following Oral Dysbiosis","authors":"Mai Nara, Mie Kurosawa, Momoe Itsumi, Hirobumi Morisaki, Haruka Fukamachi, Nobuo Okahashi, Noriyuki Suzuki, Hirotaka Kuwata","doi":"10.1111/1348-0421.13191","DOIUrl":"10.1111/1348-0421.13191","url":null,"abstract":"<p>The oral microbiome is closely involved in the maintenance of host health and the development of systemic diseases. The salivary glands play an essential role in homeostasis in the oral cavity. Here, we investigated the effects of periodontal inflammation on salivary gland function and the oral microbiome. In experimental periodontitis model mice, an increase in IgA⁺ cells in the salivary glands were observed 1 week after treatment. Alteration of the oral microbiome was also induced in this model. Gene expression analysis of the salivary glands showed changes in the expression of genes related to B-cell maturation and plasma cell differentiation and an increase in the expression of genes related to macrophage activation upon experimental periodontitis induction. Furthermore, the relationship between disruption of oral microflora and salivary gland function was examined using a cohousing model in which experimental periodontitis model mice and untreated mice were reared in the same cage. We found that cohoused normal mice underwent alteration of the oral microbiome, with increases in IgA⁺ cells and macrophages in the salivary glands. In summary, our results suggest that, in the oral cavity, there is a close link between oral bacterial flora and immune cells in the salivary glands. Our results also show that localized inflammation disrupts the homeostasis in the oral cavity, inducing pathological conditions such as dysbiosis. Our study suggests the importance of the interaction among local oral inflammation, salivary gland function, and oral microflora, and provides new insights into the mechanisms by which oral health is maintained.</p>","PeriodicalId":18679,"journal":{"name":"Microbiology and Immunology","volume":"69 2","pages":"114-127"},"PeriodicalIF":1.9,"publicationDate":"2024-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1348-0421.13191","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142872510","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Upon infection with the virus, cells increase the expression of cytidine deaminase APOBEC3 family genes. This leads to the accumulation of C-to-T mutations in the replicating viral genome and suppresses viral propagation. In contrast, herpesviruses, including Epstein–Barr virus (EBV), express genes that counteract APOBEC3 during lytic infection. However, because viral resistance factors are not expressed during EBV latent infection, it is unknown how APOBEC3 functions during latent infection. We observed that in gastric epithelial cells persistently infected with EBV, the expression of APOBEC3 family genes increased, C-to-T mutations in the D-loop genome of mitochondrial DNA (mtDNA) increased, and mtDNA copy number decreased. By introducing and expressing individual APOBEC3 family genes, APOBEC3C was particularly expressed in the cytoplasm, increasing C-to-T mutations in mtDNA and decreasing mtDNA copy number. Furthermore, we confirmed that APOBEC3C co-localized with mitochondria in EBV-infected cells. Expression of the EBV latent gene LMP2A increased APOBEC3C expression. Conversely, APOBEC3C expression was reduced in LMP2A-deficient EBV-infected cells compared to wild-type EBV-infected cells. These results indicate that persistent infection of EBV in gastric epithelial cells reduces the number of mitochondria through mtDNA mutations induced by APOBEC3C expression.
{"title":"Persistent Epstein–Barr Virus Infection of Epithelial Cells Leads to APOBEC3C Expression and Induces Mitochondrial DNA Mutations","authors":"Aung Phyo Wai, Timmy Richardo, Kousho Wakae, Shunpei Okada, Masamichi Muramatsu, Hironori Yoshiyama, Hisashi Iizasa","doi":"10.1111/1348-0421.13196","DOIUrl":"10.1111/1348-0421.13196","url":null,"abstract":"<div>\u0000 \u0000 <p>Upon infection with the virus, cells increase the expression of cytidine deaminase APOBEC3 family genes. This leads to the accumulation of C-to-T mutations in the replicating viral genome and suppresses viral propagation. In contrast, herpesviruses, including Epstein–Barr virus (EBV), express genes that counteract APOBEC3 during lytic infection. However, because viral resistance factors are not expressed during EBV latent infection, it is unknown how APOBEC3 functions during latent infection. We observed that in gastric epithelial cells persistently infected with EBV, the expression of APOBEC3 family genes increased, C-to-T mutations in the D-loop genome of mitochondrial DNA (mtDNA) increased, and mtDNA copy number decreased. By introducing and expressing individual APOBEC3 family genes, APOBEC3C was particularly expressed in the cytoplasm, increasing C-to-T mutations in mtDNA and decreasing mtDNA copy number. Furthermore, we confirmed that APOBEC3C co-localized with mitochondria in EBV-infected cells. Expression of the EBV latent gene LMP2A increased APOBEC3C expression. Conversely, APOBEC3C expression was reduced in LMP2A-deficient EBV-infected cells compared to wild-type EBV-infected cells. These results indicate that persistent infection of EBV in gastric epithelial cells reduces the number of mitochondria through mtDNA mutations induced by APOBEC3C expression.</p>\u0000 </div>","PeriodicalId":18679,"journal":{"name":"Microbiology and Immunology","volume":"69 3","pages":"157-167"},"PeriodicalIF":1.9,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142864832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The Gram-negative bacteria Bordetella pertussis, B. parapertussis, and B. bronchiseptica cause respiratory diseases in various mammals. They share the BvgAS two-component system, which regulates the phenotypic conversion between the virulent Bvg+ and avirulent Bvg– phases. In the BvgAS system, the sensor kinase BvgS senses environmental cues and transduces a phosphorelay signal to the response regulator BvgA, which leads to the expression of Bvg+ phase-specific genes, including virulence factor genes. Bacteria grown at 37°C exhibit the Bvg+ phenotype. In contrast, at lower than 26°C or in the presence of modulators, such as MgSO4 and nicotinic acid, the BvgAS system is inactivated, leading bacteria to the avirulent Bvg– phase. Therefore, effective modulators are expected to provide a therapeutic measure for Bordetella infection; however, no such modulators are currently available, and the mechanism by which modulators inactivate the BvgAS system is poorly understood. In the present study, we identified lonidamine as a novel modulator after screening an FDA-approved drug library using bacterial reporter systems with the Bvg+-specific and Bvg–-specific promoters. Lonidamine directly bound to the VFT2 domain of BvgS and inactivated the BvgAS system at concentrations as low as 50 nM, which was at least 2000- to 20,000-fold lower than the effective concentrations of known modulators. Lonidamine significantly reduced the adherence of B. pertussis to cultured cells but unexpectedly exacerbated bacterial colonization of the mouse nasal septum. These results provide insights into the structural requirements for BvgAS modulators and the role of Bvg phenotypes in the establishment of infection.
{"title":"Lonidamine, a Novel Modulator for the BvgAS System of Bordetella Species","authors":"Natsuko Ota, Takashi Nishida, Daron M. Standley, Aalaa Alrahman Sherif, Satoshi Iwano, Dendi Krisna Nugraha, Toshiya Ueno, Yasuhiko Horiguchi","doi":"10.1111/1348-0421.13193","DOIUrl":"10.1111/1348-0421.13193","url":null,"abstract":"<p>The Gram-negative bacteria <i>Bordetella pertussis</i>, <i>B. parapertussis</i>, and <i>B. bronchiseptica</i> cause respiratory diseases in various mammals. They share the BvgAS two-component system, which regulates the phenotypic conversion between the virulent Bvg<sup>+</sup> and avirulent Bvg<sup>–</sup> phases. In the BvgAS system, the sensor kinase BvgS senses environmental cues and transduces a phosphorelay signal to the response regulator BvgA, which leads to the expression of Bvg<sup>+</sup> phase-specific genes, including virulence factor genes. Bacteria grown at 37°C exhibit the Bvg<sup>+</sup> phenotype. In contrast, at lower than 26°C or in the presence of modulators, such as MgSO<sub>4</sub> and nicotinic acid, the BvgAS system is inactivated, leading bacteria to the avirulent Bvg<sup>–</sup> phase. Therefore, effective modulators are expected to provide a therapeutic measure for <i>Bordetella</i> infection; however, no such modulators are currently available, and the mechanism by which modulators inactivate the BvgAS system is poorly understood. In the present study, we identified lonidamine as a novel modulator after screening an FDA-approved drug library using bacterial reporter systems with the Bvg<sup>+</sup>-specific and Bvg<sup>–</sup>-specific promoters. Lonidamine directly bound to the VFT2 domain of BvgS and inactivated the BvgAS system at concentrations as low as 50 nM, which was at least 2000- to 20,000-fold lower than the effective concentrations of known modulators. Lonidamine significantly reduced the adherence of <i>B. pertussis</i> to cultured cells but unexpectedly exacerbated bacterial colonization of the mouse nasal septum. These results provide insights into the structural requirements for BvgAS modulators and the role of Bvg phenotypes in the establishment of infection.</p>","PeriodicalId":18679,"journal":{"name":"Microbiology and Immunology","volume":"69 3","pages":"133-147"},"PeriodicalIF":1.9,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1348-0421.13193","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142829303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Trichosporon asahii is a pathogenic fungus that causes severe deep-seated mycosis in immunocompromised patients with neutropenia. Understanding the molecular mechanisms of T. asahii infection will facilitate the development of new therapeutic and preventive strategies. Two main obstacles have prevented the identification of virulence-related genes in T. asahii using molecular genetic techniques: the lack of experimental animal infection models for easy evaluation of T. asahii virulence and the lack of genetic recombination technology for T. asahii. To address these issues, we developed a silkworm infection model to quantitatively evaluate T. asahii virulence and a genetic recombination method to generate gene-deficient T. asahii mutants, enabling the identification of virulence factors of T. asahii. In this review, we propose a strategy for identifying virulence-related factors in T. asahii using a silkworm infection model and an efficient gene-targeting system.
{"title":"Strategy to Identify Virulence-Related Genes of the Pathogenic Fungus Trichosporon asahii Using an Efficient Gene-Targeting System","authors":"Yasuhiko Matsumoto, Sanae Kurakado, Tsuyoshi Yamada, Takashi Sugita","doi":"10.1111/1348-0421.13192","DOIUrl":"10.1111/1348-0421.13192","url":null,"abstract":"<div>\u0000 \u0000 <p><i>Trichosporon asahii</i> is a pathogenic fungus that causes severe deep-seated mycosis in immunocompromised patients with neutropenia. Understanding the molecular mechanisms of <i>T. asahii</i> infection will facilitate the development of new therapeutic and preventive strategies. Two main obstacles have prevented the identification of virulence-related genes in <i>T. asahii</i> using molecular genetic techniques: the lack of experimental animal infection models for easy evaluation of <i>T. asahii</i> virulence and the lack of genetic recombination technology for <i>T. asahii</i>. To address these issues, we developed a silkworm infection model to quantitatively evaluate <i>T. asahii</i> virulence and a genetic recombination method to generate gene-deficient <i>T. asahii</i> mutants, enabling the identification of virulence factors of <i>T. asahii</i>. In this review, we propose a strategy for identifying virulence-related factors in <i>T. asahii</i> using a silkworm infection model and an efficient gene-targeting system.</p>\u0000 </div>","PeriodicalId":18679,"journal":{"name":"Microbiology and Immunology","volume":"69 2","pages":"77-84"},"PeriodicalIF":1.9,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142807483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cover photograph: Representation of the E6 + Lumacaftor (ZINC000064033452) complex. The hydrogen bonds formed (yellow dotted lines), the distance in Å of these interactions, and the residues that interact with the drug or are part of the binding site were highlighted. Microbiol Immunol: 68:414-426. Article link here
{"title":"Issue Information – Cover","authors":"","doi":"10.1111/1348-0421.13186","DOIUrl":"https://doi.org/10.1111/1348-0421.13186","url":null,"abstract":"<p><b>Cover photograph</b>: Representation of the E6 + Lumacaftor (ZINC000064033452) complex. The hydrogen bonds formed (yellow dotted lines), the distance in Å of these interactions, and the residues that interact with the drug or are part of the binding site were highlighted. <i>Microbiol Immunol: 68:414-426</i>. Article link here\u0000 \u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":18679,"journal":{"name":"Microbiology and Immunology","volume":"68 12","pages":"i-ii"},"PeriodicalIF":1.9,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1348-0421.13186","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142860803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Staphylococcus aureus is a versatile pathogen capable of causing a wide range of infections, from minor skin infections to life-threatening invasive diseases. The pathogenicity of S. aureus is attributed to its ability to produce various virulence factors, including adhesion and biofilm-related proteins. Understanding the prevalence and distribution of these genes among S. aureus isolates from different sources is crucial for devising effective strategies to combat biofilm-associated contamination. In this study, we conducted a comprehensive network meta-analysis to assess the prevalence of adhesion and biofilm-related genes in S. aureus isolates and investigate the impact of the isolate source on their occurrence. A systematic search of multiple databases was performed, and a total of 53 relevant studies were included. The prevalence of adhesion and biofilm-related genes in S. aureus isolates was determined, with the highest prevalence observed for clfB (p-estimate = 85.4, 95% confidence interval [CI] 78–90.6), followed by eno (p-estimate = 81.1, 95% CI 61.7–91.9), and icaD (p-estimate = 77, 95% CI 68.6–83.6). Conversely, bap and bbp genes exhibited the lowest prevalence rates (p-estimate = 6.7 and 18.7, respectively). The network meta-analysis allowed us to examine the pairwise co-study of adhesion and biofilm-related genes in S. aureus isolates. The most frequently co-studied gene pairs were icaA-icaD (30 times) and fnbA-fnbB (25 times). Subgroup analysis showed that the occurrence of icaC and icaB genes was significantly lower in animal isolates compared to human and food isolates (p < 0.05). It is worth noting that there was limited data available for the analysis of sasG, bbp, bap, eno, and fib genes. In conclusion, the study revealed varying prevalence rates of adhesion and biofilm-related genes in S. aureus isolates. Genes such as clfB, eno, and icaD were found to be highly prevalent, while bap and bbp were less common. Limited existing data on the prevalence of genes like sasG, bbp, bap, eno, and fib highlights the need for further research to determine their exact prevalence rates. Our results contribute to a better understanding of S. aureus pathogenesis and can facilitate the development of effective strategies for the prevention and treatment of S. aureus infections.
金黄色葡萄球菌是一种多功能病原体，能够引起广泛的感染，从轻微的皮肤感染到危及生命的侵袭性疾病。金黄色葡萄球菌的致病性归因于其产生各种毒力因子的能力，包括粘附和生物膜相关蛋白。了解这些基因在不同来源的金黄色葡萄球菌分离株中的流行和分布对于制定有效的策略来对抗生物膜相关污染至关重要。在这项研究中，我们进行了一项全面的网络荟萃分析，以评估金黄色葡萄球菌分离株中粘附和生物膜相关基因的患病率，并研究分离源对其发生的影响。系统检索多个数据库，共纳入53项相关研究。测定了金黄色葡萄球菌分离株中粘附和生物膜相关基因的患病率，其中clfB的患病率最高（p-估计= 85.4,95%可信区间[CI] 78-90.6），其次是eno （p-估计= 81.1,95% CI 61.7-91.9）和icaD （p-估计= 77,95% CI 68.6-83.6）。相反，bap和bbp基因的患病率最低（p-estimate分别为6.7和18.7）。网络荟萃分析使我们能够检查金黄色葡萄球菌分离株中粘附和生物膜相关基因的两两共同研究。共同研究次数最多的基因对是icaA-icaD（30次）和fnbA-fnbB（25次）。亚组分析显示，与人类和食物分离株相比，动物分离株中icaC和icaB基因的发生率显著降低
{"title":"The Prevalence and Comparative Analysis of Adhesion and Biofilm-Related Genes in Staphylococcus aureus Isolates: A Network Meta-Analysis","authors":"Aram Sharifi, Peyman Mahmoudi, Keyvan Sobhani, Morahem Ashengroph","doi":"10.1111/1348-0421.13189","DOIUrl":"10.1111/1348-0421.13189","url":null,"abstract":"<p><i>Staphylococcus aureus</i> is a versatile pathogen capable of causing a wide range of infections, from minor skin infections to life-threatening invasive diseases. The pathogenicity of <i>S. aureus</i> is attributed to its ability to produce various virulence factors, including adhesion and biofilm-related proteins. Understanding the prevalence and distribution of these genes among <i>S. aureus</i> isolates from different sources is crucial for devising effective strategies to combat biofilm-associated contamination. In this study, we conducted a comprehensive network meta-analysis to assess the prevalence of adhesion and biofilm-related genes in <i>S. aureus</i> isolates and investigate the impact of the isolate source on their occurrence. A systematic search of multiple databases was performed, and a total of 53 relevant studies were included. The prevalence of adhesion and biofilm-related genes in <i>S. aureus</i> isolates was determined, with the highest prevalence observed for <i>clfB</i> (<i>p</i>-estimate = 85.4, 95% confidence interval [CI] 78–90.6), followed by <i>eno</i> (<i>p</i>-estimate = 81.1, 95% CI 61.7–91.9), and <i>icaD</i> (<i>p</i>-estimate = 77, 95% CI 68.6–83.6). Conversely, <i>bap</i> and <i>bbp</i> genes exhibited the lowest prevalence rates (<i>p</i>-estimate = 6.7 and 18.7, respectively). The network meta-analysis allowed us to examine the pairwise co-study of adhesion and biofilm-related genes in <i>S. aureus</i> isolates. The most frequently co-studied gene pairs were <i>icaA</i>-<i>icaD</i> (30 times) and <i>fnbA</i>-<i>fnbB</i> (25 times). Subgroup analysis showed that the occurrence of <i>icaC</i> and <i>icaB</i> genes was significantly lower in animal isolates compared to human and food isolates (<i>p</i> < 0.05). It is worth noting that there was limited data available for the analysis of <i>sasG</i>, <i>bbp</i>, <i>bap</i>, <i>eno</i>, and <i>fib</i> genes. In conclusion, the study revealed varying prevalence rates of adhesion and biofilm-related genes in <i>S. aureus</i> isolates. Genes such as <i>clfB</i>, <i>eno</i>, and <i>icaD</i> were found to be highly prevalent, while <i>bap</i> and <i>bbp</i> were less common. Limited existing data on the prevalence of genes like <i>sasG</i>, <i>bbp</i>, <i>bap</i>, <i>eno</i>, and <i>fib</i> highlights the need for further research to determine their exact prevalence rates. Our results contribute to a better understanding of <i>S. aureus</i> pathogenesis and can facilitate the development of effective strategies for the prevention and treatment of <i>S. aureus</i> infections.</p>","PeriodicalId":18679,"journal":{"name":"Microbiology and Immunology","volume":"69 2","pages":"104-113"},"PeriodicalIF":1.9,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142786315","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hepatitis B virus (HBV) infection is a serious global health problem causing acute and chronic hepatitis and related diseases. Approximately, 296 million patients have been chronically infected with the virus, leading to cirrhosis and hepatocellular carcinoma. Although HBV polymerase (HBVpol, pol) plays a pivotal role in HBV replication and must be a definite therapeutic target. The problems are that the detailed functions and intracellular dynamics of HBVpol remain unclear. Here, we constructed two kinds of tagged HBVpol, PA-tagged and HiBiT-tagged pol, and the HBV-producing vectors. Each PA tag and HiBiT tag were inserted into N-terminus of spacer region on HBVpol open reading frame. Transfection of the plasmids into HepG2 cells led to production of HBV. These tagged HBVpol were detectable in HBV replicating cells and pol-HiBiT enabled quantitative analysis. Furthermore, these recombinant HBV were infectious to primary human hepatocytes. Thus, we successfully designed infectious and replication-competent recombinant HBV harboring detectable tagged HBVpol. Such infectious recombinant HBV will provide a novel tool to study HBVpol dynamics and develop new therapeutics against HBV.
{"title":"Generation of Replication-Competent Hepatitis B Virus Harboring Tagged Polymerase for Visualization and Quantification of the Infection","authors":"Chiharu Morita, Masami Wada, Eriko Ohsaki, Shihoko Kimura-Ohba, Keiji Ueda","doi":"10.1111/1348-0421.13183","DOIUrl":"10.1111/1348-0421.13183","url":null,"abstract":"<p>Hepatitis B virus (HBV) infection is a serious global health problem causing acute and chronic hepatitis and related diseases. Approximately, 296 million patients have been chronically infected with the virus, leading to cirrhosis and hepatocellular carcinoma. Although HBV polymerase (HBVpol, pol) plays a pivotal role in HBV replication and must be a definite therapeutic target. The problems are that the detailed functions and intracellular dynamics of HBVpol remain unclear. Here, we constructed two kinds of tagged HBVpol, PA-tagged and HiBiT-tagged pol, and the HBV-producing vectors. Each PA tag and HiBiT tag were inserted into N-terminus of spacer region on HBVpol open reading frame. Transfection of the plasmids into HepG2 cells led to production of HBV. These tagged HBVpol were detectable in HBV replicating cells and pol-HiBiT enabled quantitative analysis. Furthermore, these recombinant HBV were infectious to primary human hepatocytes. Thus, we successfully designed infectious and replication-competent recombinant HBV harboring detectable tagged HBVpol. Such infectious recombinant HBV will provide a novel tool to study HBVpol dynamics and develop new therapeutics against HBV.</p>","PeriodicalId":18679,"journal":{"name":"Microbiology and Immunology","volume":"69 1","pages":"43-58"},"PeriodicalIF":1.9,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1348-0421.13183","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142769988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jiwei Wang, Jixin He, Dandan Liu, Tao Zhang, Yin Wu, Ming Xie
Functional constipation (FC) is a common digestive disorder that affects patients' quality of life and is closely associated with intestinal tumors. This study used a cross-sectional design to assess the changes of intestinal flora and metabolites in different severities of FC patients through 16S rRNA sequencing and metabolomics analysis. Results showed that patients with severe FC had significantly higher clinical and anxiety scores compared to those in the mild and moderate groups. The species richness of intestinal microorganisms in the severe FC group was also significantly higher, and obvious differences in the flora composition existed. Specifically, the Bacteroidota was more abundant in the severe FC group, which was a characteristic feature distinguishing severe FC. Metabolomic analyses also revealed metabolite differences among patients with mild-to-moderate and severe FC, with the severe FC group showing increased enrichment in L-isoleucine biosynthesis and glycolysis metabolic pathways. The short-chain fatty acid–targeted metabolome suggested that a decrease in butyric acid might be related to worsening constipation. This study suggests that specific flora and metabolic pathways could serve as potential diagnostic and therapeutic targets, thereby contributing to the development of new diagnostic and therapeutic approaches to improve the quality of life and therapeutic outcomes for FC patients.
{"title":"Gut Microbiota and Metabolite Profiles Associated With Functional Constipation Severity","authors":"Jiwei Wang, Jixin He, Dandan Liu, Tao Zhang, Yin Wu, Ming Xie","doi":"10.1111/1348-0421.13187","DOIUrl":"10.1111/1348-0421.13187","url":null,"abstract":"<p>Functional constipation (FC) is a common digestive disorder that affects patients' quality of life and is closely associated with intestinal tumors. This study used a cross-sectional design to assess the changes of intestinal flora and metabolites in different severities of FC patients through 16S rRNA sequencing and metabolomics analysis. Results showed that patients with severe FC had significantly higher clinical and anxiety scores compared to those in the mild and moderate groups. The species richness of intestinal microorganisms in the severe FC group was also significantly higher, and obvious differences in the flora composition existed. Specifically, the <i>Bacteroidota</i> was more abundant in the severe FC group, which was a characteristic feature distinguishing severe FC. Metabolomic analyses also revealed metabolite differences among patients with mild-to-moderate and severe FC, with the severe FC group showing increased enrichment in L-isoleucine biosynthesis and glycolysis metabolic pathways. The short-chain fatty acid–targeted metabolome suggested that a decrease in butyric acid might be related to worsening constipation. This study suggests that specific flora and metabolic pathways could serve as potential diagnostic and therapeutic targets, thereby contributing to the development of new diagnostic and therapeutic approaches to improve the quality of life and therapeutic outcomes for FC patients.</p>","PeriodicalId":18679,"journal":{"name":"Microbiology and Immunology","volume":"69 2","pages":"85-95"},"PeriodicalIF":1.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142769948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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