cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.27003414.v1
title: Insect hypovirulence-associated mycovirus confers entomopathogenic fungi with enhanced resistance against phytopathogens

description: Mycoviruses can alter the biological characteristics of host fungi, including change virulence or pathogenicity of phytopathogens and entomopathogenic fungi (EPF). However, most studies on the mycoviruses found in EPF have focused on the effects of the viruses on the virulence of host fungi towards insect pests, with relatively few reports on the effects to the host fungi with regard to plant disease resistance in hosts. The present study investigated the effects of the mycovirus <i>Beauveria bassiana</i> chrysovirus 2 (BbCV2) virus infection on host biological characteristics, evaluated antagonistic activity of BbCV2 against two phytopathogenic fungi (<i>Sclerotinia sclerotiorum</i> and <i>Botrytis cinerea</i>), and transcriptome analysis was used to reveal the interactions between viruses and hosts. Our results showed that BbCV2 virus infection increased <i>B. bassiana</i>‘s growth rate, spore production, and biomass, it also enhanced the capacity of host fungi and their metabolic products to inhibit phytopathogenic fungi. BbCV2 virus infection reduced the contents of the two pathogens in tomato plants significantly, and transcriptome analysis revealed that the genes related to competition for ecological niches and nutrition, mycoparasitism and secondary metabolites in <i>B. bassiana</i> were significantly up-regulated after viral infection. These findings indicated that the mycovirus infection is an important factor to enhance the ability of <i>B. bassiana</i> against plant disease after endophytic colonization. We suggest that mycovirus infection causes a positive effect on <i>B. bassiana</i> against phytopathogens, which should be considered as a potential strategy to promote the plant disease resistance of EPF.
DOI: 10.6084/m9.figshare.25449464.v1
title: Iron depletion has different consequences on the growth and survival of <i>Toxoplasma gondii</i> strains

description: <i>Toxoplasma gondii</i> is an obligate intracellular parasite responsible for a pathology called toxoplasmosis, which primarily affects immunocompromised individuals and developing foetuses. The parasite can scavenge essential nutrients from its host to support its growth and survival. Among them, iron is one of the most important elements needed to sustain basic cellular functions as it is involved in a number of key metabolic processes, including oxygen transport, redox balance, and electron transport. We evaluated the effects of an iron chelator on the development of several parasite strains and found that they differed in their ability to tolerate iron depletion. The growth of parasites usually associated with a model of acute toxoplasmosis was strongly affected by iron depletion, whereas cystogenic strains were less sensitive as they were able to convert into persisting developmental forms that are associated with the chronic form of the disease. Ultrastructural and biochemical characterization of the impact of iron depletion on parasites also highlighted striking changes in both their metabolism and that of the host, with a marked accumulation of lipid droplets and perturbation of lipid homoeostasis. Overall, our study demonstrates that although acute iron depletion has an important effect on the growth of <i>T. gondii</i>, it has a more profound impact on actively dividing parasites, whereas less metabolically active parasite forms may be able to avoid some of the most detrimental consequences.
DOI: 10.6084/m9.figshare.26892519
title: Simulating the clinical manifestations and disease progression of human sepsis: A monobacterial injection approach for animal modeling

description: Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection, with great clinical heterogeneity, high morbidity, and high mortality. At the same time, there are many kinds of infection sources, the pathophysiology is very complex, and the pathogenesis has not been fully elucidated. An ideal animal model of sepsis can accurately simulate clinical sepsis and promote the development of sepsis-related pathogenesis, treatment methods, and prognosis. The existing sepsis model still uses the previous Sepsis 2.0 modelling standard, which has some problems, such as many kinds of infection sources, poor repeatability, inability to take into account single-factor studies, and large differences from clinical sepsis patients. To solve these problems, this study established a new animal model of sepsis. The model uses intravenous tail injection of a single bacterial strain, simplifying the complexity of multibacterial infection, and effectively solving the above problems.
DOI: 10.6084/m9.figshare.27003414
title: Insect hypovirulence-associated mycovirus confers entomopathogenic fungi with enhanced resistance against phytopathogens

description: Mycoviruses can alter the biological characteristics of host fungi, including change virulence or pathogenicity of phytopathogens and entomopathogenic fungi (EPF). However, most studies on the mycoviruses found in EPF have focused on the effects of the viruses on the virulence of host fungi towards insect pests, with relatively few reports on the effects to the host fungi with regard to plant disease resistance in hosts. The present study investigated the effects of the mycovirus <i>Beauveria bassiana</i> chrysovirus 2 (BbCV2) virus infection on host biological characteristics, evaluated antagonistic activity of BbCV2 against two phytopathogenic fungi (<i>Sclerotinia sclerotiorum</i> and <i>Botrytis cinerea</i>), and transcriptome analysis was used to reveal the interactions between viruses and hosts. Our results showed that BbCV2 virus infection increased <i>B. bassiana</i>‘s growth rate, spore production, and biomass, it also enhanced the capacity of host fungi and their metabolic products to inhibit phytopathogenic fungi. BbCV2 virus infection reduced the contents of the two pathogens in tomato plants significantly, and transcriptome analysis revealed that the genes related to competition for ecological niches and nutrition, mycoparasitism and secondary metabolites in <i>B. bassiana</i> were significantly up-regulated after viral infection. These findings indicated that the mycovirus infection is an important factor to enhance the ability of <i>B. bassiana</i> against plant disease after endophytic colonization. We suggest that mycovirus infection causes a positive effect on <i>B. bassiana</i> against phytopathogens, which should be considered as a potential strategy to promote the plant disease resistance of EPF.
DOI: 10.6084/m9.figshare.27939998
title: Exploring the dynamics of gut microbiota, antibiotic resistance, and chemotherapy impact in acute leukemia patients: A comprehensive metagenomic analysis

description: Leukemia poses significant challenges to its treatment, and understanding its complex pathogenesis is crucial. This study used metagenomic sequencing to investigate the interplay between chemotherapy, gut microbiota, and antibiotic resistance in patients with acute leukemia (AL). Pre- and post-chemotherapy stool samples from patients revealed alterations in microbial richness, taxa, and antibiotic resistance genes (ARGs). The analysis revealed a decreased alpha diversity, increased dispersion in post-chemotherapy samples, and changes in the abundance of specific bacteria. Key bacteria such as <i>Enterococcus, Klebsiella</i>, and <i>Escherichia coli have</i> been identified as prevalent ARG carriers. Correlation analysis between gut microbiota and blood indicators revealed potential links between microbial species and inflammatory biomarkers, including C-reactive protein (CRP) and adenosine deaminase (ADA). This study investigated the impact of antibiotic dosage on microbiota and ARGs, revealing networks connecting co-occurring ARGs with microbial species (179 nodes, 206 edges), and networks associated with ARGs and antibiotic dosages (50 nodes, 50 edges). Antibiotics such as cephamycin and sulfonamide led to multidrug-resistant <i>Klebsiella</i> colonization. Our analyses revealed distinct microbial profiles with <i>Salmonella enterica</i> elevated post-chemotherapy in NF patients and <i>Akkermansia muciniphila</i> elevated pre-chemotherapy. These microbial signatures could inform strategies to modulate the gut microbiome, potentially mitigating the risk of neutropenic fever in patients undergoing chemotherapy. Finally, a comprehensive analysis of KEGG modules shed light on disrupted metabolic pathways after chemotherapy, providing insights into potential targets for managing side effects. Overall, this study revealed intricate relationships between gut microbiota, chemotherapy, and antibiotic resistance, providing new insights into improving therapy and enhancing patient outcomes.
DOI: 10.6084/m9.figshare.27939998.v1
title: Exploring the dynamics of gut microbiota, antibiotic resistance, and chemotherapy impact in acute leukemia patients: A comprehensive metagenomic analysis

description: Leukemia poses significant challenges to its treatment, and understanding its complex pathogenesis is crucial. This study used metagenomic sequencing to investigate the interplay between chemotherapy, gut microbiota, and antibiotic resistance in patients with acute leukemia (AL). Pre- and post-chemotherapy stool samples from patients revealed alterations in microbial richness, taxa, and antibiotic resistance genes (ARGs). The analysis revealed a decreased alpha diversity, increased dispersion in post-chemotherapy samples, and changes in the abundance of specific bacteria. Key bacteria such as <i>Enterococcus, Klebsiella</i>, and <i>Escherichia coli have</i> been identified as prevalent ARG carriers. Correlation analysis between gut microbiota and blood indicators revealed potential links between microbial species and inflammatory biomarkers, including C-reactive protein (CRP) and adenosine deaminase (ADA). This study investigated the impact of antibiotic dosage on microbiota and ARGs, revealing networks connecting co-occurring ARGs with microbial species (179 nodes, 206 edges), and networks associated with ARGs and antibiotic dosages (50 nodes, 50 edges). Antibiotics such as cephamycin and sulfonamide led to multidrug-resistant <i>Klebsiella</i> colonization. Our analyses revealed distinct microbial profiles with <i>Salmonella enterica</i> elevated post-chemotherapy in NF patients and <i>Akkermansia muciniphila</i> elevated pre-chemotherapy. These microbial signatures could inform strategies to modulate the gut microbiome, potentially mitigating the risk of neutropenic fever in patients undergoing chemotherapy. Finally, a comprehensive analysis of KEGG modules shed light on disrupted metabolic pathways after chemotherapy, providing insights into potential targets for managing side effects. Overall, this study revealed intricate relationships between gut microbiota, chemotherapy, and antibiotic resistance, providing new insights into improving therapy and enhancing patient outcomes.
DOI: 10.6084/m9.figshare.26892519.v1
title: Simulating the clinical manifestations and disease progression of human sepsis: A monobacterial injection approach for animal modeling

description: Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection, with great clinical heterogeneity, high morbidity, and high mortality. At the same time, there are many kinds of infection sources, the pathophysiology is very complex, and the pathogenesis has not been fully elucidated. An ideal animal model of sepsis can accurately simulate clinical sepsis and promote the development of sepsis-related pathogenesis, treatment methods, and prognosis. The existing sepsis model still uses the previous Sepsis 2.0 modelling standard, which has some problems, such as many kinds of infection sources, poor repeatability, inability to take into account single-factor studies, and large differences from clinical sepsis patients. To solve these problems, this study established a new animal model of sepsis. The model uses intravenous tail injection of a single bacterial strain, simplifying the complexity of multibacterial infection, and effectively solving the above problems.
DOI: 10.6084/m9.figshare.27158951
title: The roles of cell wall inhibition responsive protein CwrA in the pathogenicity of <i>Staphylococcus aureus</i>

description: The ability to form robust biofilms and secrete a diverse array of virulence factors are key pathogenic determinants of <i>Staphylococcus aureus</i>, causing a wide range of infectious diseases. Here, we characterized <i>cwrA</i> as a VraR-regulated gene encoding a cell wall inhibition-responsive protein (CwrA) using electrophoretic mobility shift assays. We constructed <i>cwrA</i> deletion mutants in the genetic background of methicillin-resistant <i>S. aureus</i> (MRSA) and methicillin-sensitive <i>S. aureus</i> (MSSA) strains. Phenotypic analyses indicated that deletion of <i>cwrA</i> led to impaired biofilm formation, which was correlated with polysaccharide intercellular adhesin (PIA). Besides, the results of real-time quantitative PCR (RT-qPCR) and β-galactosidase activity assay revealed that CwrA promoted biofilm formation by influence the <i>ica</i> operon activity in <i>S. aureus</i>. Furthermore, <i>cwrA</i> deletion mutants released less extracellular DNA (eDNA) in the biofilm because of their reduced autolytic activity compared to the wild-type (WT) strains. We also found that <i>cwrA</i> deletion mutant more virulence than the parental strain because of its enhanced hemolytic activity. Mechanistically, this phenotypic alteration is related to activation of the SaeRS two-component system, which positively regulates the transcriptional levels of genes encoding membrane-damaging toxins. Overall, our results suggest that CwrA plays an important role in modulating biofilm formation and hemolytic activity in <i>S. aureus</i>.
DOI: 10.6084/m9.figshare.27158951.v2
title: The roles of cell wall inhibition responsive protein CwrA in the pathogenicity of <i>Staphylococcus aureus</i>

description: The ability to form robust biofilms and secrete a diverse array of virulence factors are key pathogenic determinants of <i>Staphylococcus aureus</i>, causing a wide range of infectious diseases. Here, we characterized <i>cwrA</i> as a VraR-regulated gene encoding a cell wall inhibition-responsive protein (CwrA) using electrophoretic mobility shift assays. We constructed <i>cwrA</i> deletion mutants in the genetic background of methicillin-resistant <i>S. aureus</i> (MRSA) and methicillin-sensitive <i>S. aureus</i> (MSSA) strains. Phenotypic analyses indicated that deletion of <i>cwrA</i> led to impaired biofilm formation, which was correlated with polysaccharide intercellular adhesin (PIA). Besides, the results of real-time quantitative PCR (RT-qPCR) and β-galactosidase activity assay revealed that CwrA promoted biofilm formation by influence the <i>ica</i> operon activity in <i>S. aureus</i>. Furthermore, <i>cwrA</i> deletion mutants released less extracellular DNA (eDNA) in the biofilm because of their reduced autolytic activity compared to the wild-type (WT) strains. We also found that <i>cwrA</i> deletion mutant more virulence than the parental strain because of its enhanced hemolytic activity. Mechanistically, this phenotypic alteration is related to activation of the SaeRS two-component system, which positively regulates the transcriptional levels of genes encoding membrane-damaging toxins. Overall, our results suggest that CwrA plays an important role in modulating biofilm formation and hemolytic activity in <i>S. aureus</i>.
DOI: 10.6084/m9.figshare.26861070
title: The presence of differentiated C2C12 muscle cells enhances toxin production and growth by <i>Clostridium perfringens</i> type A strain ATCC3624

description: <i>Clostridium perfringens</i> type A causes gas gangrene, which involves muscle infection. Both alpha toxin (PLC), encoded by the <i>plc</i> gene, and perfringolysin O (PFO), encoded by the <i>pfoA</i> gene, are important when type A strains cause gas gangrene in a mouse model. This study used the differentiated C2C12 muscle cell line to test the hypothesis that one or both of those toxins contributes to gas gangrene pathogenesis by releasing growth nutrients from muscle cells. RT-qPCR analyses showed that the presence of differentiated C2C12 cells induces <i>C. perfringens</i> type A strain ATCC3624 to upregulate <i>plc</i> and <i>pfoA</i> expression, as well as increase expression of several regulatory genes, including <i>virS/R</i>, <i>agrB/D</i>, and <i>eutV/W</i>. The VirS/R two component regulatory system (TCRS) and its coupled Agr-like quorum sensing system, along with the EutV/W TCRS (which regulates expression of genes involved in ethanolamine [EA] utilization), were shown to mediate the C2C12 cell-induced increase in <i>plc</i> and <i>pfoA</i> expression. EA was demonstrated to increase toxin gene expression. ATCC3624 growth increased in the presence of differentiated C2C12 muscle cells and this effect was shown to involve both PFO and PLC. Those membrane-active toxins were each cytotoxic for differentiated C2C12 cells, suggesting they support ATCC3624 growth by releasing nutrients from differentiated C2C12 cells. These findings support a model where, during gas gangrene, increased production of PFO and PLC in the presence of muscle cells causes more damage to those host cells, which release nutrients like EA that are then used to support <i>C. perfringens</i> growth in muscle.
DOI: 10.6084/m9.figshare.26861070.v1
title: The presence of differentiated C2C12 muscle cells enhances toxin production and growth by <i>Clostridium perfringens</i> type A strain ATCC3624

description: <i>Clostridium perfringens</i> type A causes gas gangrene, which involves muscle infection. Both alpha toxin (PLC), encoded by the <i>plc</i> gene, and perfringolysin O (PFO), encoded by the <i>pfoA</i> gene, are important when type A strains cause gas gangrene in a mouse model. This study used the differentiated C2C12 muscle cell line to test the hypothesis that one or both of those toxins contributes to gas gangrene pathogenesis by releasing growth nutrients from muscle cells. RT-qPCR analyses showed that the presence of differentiated C2C12 cells induces <i>C. perfringens</i> type A strain ATCC3624 to upregulate <i>plc</i> and <i>pfoA</i> expression, as well as increase expression of several regulatory genes, including <i>virS/R</i>, <i>agrB/D</i>, and <i>eutV/W</i>. The VirS/R two component regulatory system (TCRS) and its coupled Agr-like quorum sensing system, along with the EutV/W TCRS (which regulates expression of genes involved in ethanolamine [EA] utilization), were shown to mediate the C2C12 cell-induced increase in <i>plc</i> and <i>pfoA</i> expression. EA was demonstrated to increase toxin gene expression. ATCC3624 growth increased in the presence of differentiated C2C12 muscle cells and this effect was shown to involve both PFO and PLC. Those membrane-active toxins were each cytotoxic for differentiated C2C12 cells, suggesting they support ATCC3624 growth by releasing nutrients from differentiated C2C12 cells. These findings support a model where, during gas gangrene, increased production of PFO and PLC in the presence of muscle cells causes more damage to those host cells, which release nutrients like EA that are then used to support <i>C. perfringens</i> growth in muscle.
DOI: 10.6084/m9.figshare.27158951.v1
title: The roles of cell wall inhibition responsive protein CwrA in the pathogenicity of staphylococcus aureus

description: The ability to form robust biofilms and secrete a diverse array of virulence factors are key pathogenic determinants of <i>Staphylococcus aureus</i>, causing a wide range of infectious diseases. Here, we characterized <i>cwrA</i> as a VraR-regulated gene encoding a cell wall inhibition-responsive protein (CwrA) using electrophoretic mobility shift assays. We constructed <i>cwrA</i> deletion mutants in the genetic background of methicillin-resistant <i>S. aureus</i> (MRSA) and methicillin-sensitive <i>S. aureus</i> (MSSA) strains. Phenotypic analyses indicated that deletion of <i>cwrA</i> led to impaired biofilm formation, which was correlated with polysaccharide intercellular adhesin (PIA). Besides, the results of real-time quantitative PCR (RT-qPCR) and β-galactosidase activity assay revealed that CwrA promoted biofilm formation by influence the <i>ica</i> operon activity in <i>S. aureus</i>. Furthermore, <i>cwrA</i> deletion mutants released less extracellular DNA (eDNA) in the biofilm because of their reduced autolytic activity compared to the wild-type (WT) strains. We also found that <i>cwrA</i> deletion mutant more virulence than the parental strain because of its enhanced haemolytic activity. Mechanistically, this phenotypic alteration is related to activation of the SaeRS two-component system, which positively regulates the transcriptional levels of genes encoding membrane-damaging toxins. Overall, our results suggest that CwrA plays an important role in modulating biofilm formation and haemolytic activity in <i>S. aureus</i>.
DOI: 10.6084/m9.figshare.27930868
title: <i>Peptostreptococcus Anaerobius</i> enhances dextran sulfate sodium-induced colitis by promoting nf-κB-NLRP3-Dependent macrophage pyroptosis

description: Evidence indicates that gut microbiota is crucial in ulcerative colitis (UC) development. Increased <i>Peptostreptococcus</i> species abundance is linked to UC, but its role and mechanisms in intestinal inflammation are not well understood. This study used a dextran sulfate sodium (DSS)-induced colitis model in mice, and different bacterial strains were administered via gavage. We assessed clinical manifestations, colonic barrier function, gut microbiota composition, and levels of inflammatory cytokines, NOD-like receptor family pyrin domain-containing 3 (NLRP3) signaling molecules, and pyroptosis-related proteins. Mouse bone marrow-derived macrophages (BMDMs) were infected with <i>Peptostreptococcus anaerobius</i> at different time points and multiplicities of infection (MOI). Cell viability and the expression of NLRP3 signaling molecules and pyroptosis-associated proteins were assessed. The inhibitors C29, TAK-242, and MCC950 were employed for Toll-like receptor (TLR) and NLRP3 signaling pathways. It was observed that <i>P. anaerobius</i> exacerbated intestinal inflammation and barrier injury in DSS-induced colitis in mice. Additionally, <i>P. anaerobius</i> contributed to gut microbiota dysbiosis during colitis progression. <i>P. anaerobius</i> induced the expression of NLRP3 signaling molecules and pyroptosis-associated proteins in mouse colitis tissues. <i>In vitro</i> assays demonstrated that <i>P. anaerobius</i> activated NLRP3 inflammasome and evoked gasdermin D-mediated pyroptosis and interleukin (IL)-1β secretion in macrophages. Furthermore, TLR2 and TLR4 were identified as key mediators of <i>P. anaerobius</i>-induced macrophage pyroptosis via activation of the Nuclear Factor-kappa B (NF-κB)-NLRP3 pathway. In conclusion, <i>P. anaerobius</i> promotes macrophage pyroptosis and IL-1β secretion through the TLR2/4-NF-κB-NLRP3 signaling axis, thereby aggravating colitis. <i>P. anaerobius</i> may represent a potential risk factor for UC development.