cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.29254332
title: Fungal β-glucan instructed miR-32-5p modulates Dectin-1 signaling mediated inflammation, reactive oxygen species and apoptosis through polarization of “M2a-like” macrophage in <i>Candida</i> colitis

description: Ulcerative colitis (UC) is a chronic and easy-to-relapse intestinal disease characterized by colon inflammation and microbial dysbiosis. <i>Candida albicans</i> is the most common fungal resident in the human gut. Overgrowth of <i>C. albicans</i> has been linked to the aggravation of UC. Previously, we demonstrated that miR-32-5p was the most differentially expressed microRNA in DSS-induced colitis model supplemented with <i>C. albicans</i> and might be a potential target in the treatment of <i>Candida</i> colitis. However, the underlying pathogenic and therapeutic mechanisms remain unclear. Here, we firstly used the ITS technique to analyse intestinal mycobiota. The miR-32-5p adenovirus in company with extracted <i>Candida</i> cell wall β-glucan were then employed to monitor the impacts of miR-32-5p and fungal β-glucan on the severity of <i>Candida</i> colitis. Subsequently, gene silencing together with inhibitors of reactive oxygen species (ROS) and apoptosis was used to survey the modulation of miR-32-5p on macrophage polarization. According to these results, <i>C. albicans</i> became the dominant intestinal fungal species in <i>Candida</i> colitis model. <i>Candida</i> β-glucan could instruct miR-32-5p expression to affect the severity of <i>Candida</i> colitis in a concentration-dependent manner. Interestingly, high fungal β-glucan with pro-inflammatory effects hindered further increases in gut inflammation. Further analysis showed that overexpression of miR-32-5p could effectively inhibit inflammation and apoptosis and enhance phagocytosis and ROS production through Dectin-1 signalling in macrophages. A panel of representative gene expressions verified the polarization of the M2-like phenotype induced by miR-32-5p. Mechanistically, our results reveal the therapeutic potential of miR-32-5p in the amelioration of <i>Candida</i> colitis.
DOI: 10.6084/m9.figshare.29254332.v1
title: Fungal β-glucan instructed miR-32-5p modulates Dectin-1 signaling mediated inflammation, reactive oxygen species and apoptosis through polarization of “M2a-like” macrophage in <i>Candida</i> colitis

description: Ulcerative colitis (UC) is a chronic and easy-to-relapse intestinal disease characterized by colon inflammation and microbial dysbiosis. <i>Candida albicans</i> is the most common fungal resident in the human gut. Overgrowth of <i>C. albicans</i> has been linked to the aggravation of UC. Previously, we demonstrated that miR-32-5p was the most differentially expressed microRNA in DSS-induced colitis model supplemented with <i>C. albicans</i> and might be a potential target in the treatment of <i>Candida</i> colitis. However, the underlying pathogenic and therapeutic mechanisms remain unclear. Here, we firstly used the ITS technique to analyse intestinal mycobiota. The miR-32-5p adenovirus in company with extracted <i>Candida</i> cell wall β-glucan were then employed to monitor the impacts of miR-32-5p and fungal β-glucan on the severity of <i>Candida</i> colitis. Subsequently, gene silencing together with inhibitors of reactive oxygen species (ROS) and apoptosis was used to survey the modulation of miR-32-5p on macrophage polarization. According to these results, <i>C. albicans</i> became the dominant intestinal fungal species in <i>Candida</i> colitis model. <i>Candida</i> β-glucan could instruct miR-32-5p expression to affect the severity of <i>Candida</i> colitis in a concentration-dependent manner. Interestingly, high fungal β-glucan with pro-inflammatory effects hindered further increases in gut inflammation. Further analysis showed that overexpression of miR-32-5p could effectively inhibit inflammation and apoptosis and enhance phagocytosis and ROS production through Dectin-1 signalling in macrophages. A panel of representative gene expressions verified the polarization of the M2-like phenotype induced by miR-32-5p. Mechanistically, our results reveal the therapeutic potential of miR-32-5p in the amelioration of <i>Candida</i> colitis.
DOI: 10.6084/m9.figshare.30577011
title: Severe fever with thrombocytopenia syndrome virus infection induces thymic atrophy in IFNAR<sup>−/−</sup> mice

description: Severe fever with thrombocytopenia syndrome virus (SFTSV) causes severe disease in humans, yet the pathogenesis remains poorly understood. A hallmark of fatal SFTS cases is the marked depletion of T cells. Previous studies on T cell depletion have predominantly focused on alterations in blood and peripheral lymphoid organs, while the thymus, a critical site for T cell development, has remained largely overlooked. In this study, we employed a lethal murine infection model to investigate the impact of SFTSV on thymic function. Our results revealed that SFTSV infected the thymus and induced severe cortical atrophy in type I interferon receptor-deficient (IFNAR<sup>−/−</sup>) mice, characterized by a dramatic depletion of CD4<sup>+</sup>CD8<sup>+</sup> double-positive (DP) thymocytes. Transcriptomic analysis indicated that thymic damage is likely attributable to impaired thymocyte proliferation and increased apoptosis, which may be a consequence of SFTSV-induced alterations in the thymic microenvironment. We found SFTSV-infected macrophages and dendritic cells in the thymus, which accumulated in the cortex and exhibited elevated secretion of IFN-γ, a cytokine commonly associated with acute thymic atrophy. These results demonstrate thymic atrophy caused by SFTSV infection and suggest potential therapeutic strategies for restoring thymic function and promoting T cell reconstitution.
DOI: 10.6084/m9.figshare.30577011.v1
title: Severe fever with thrombocytopenia syndrome virus infection induces thymic atrophy in IFNAR<sup>−/−</sup> mice

description: Severe fever with thrombocytopenia syndrome virus (SFTSV) causes severe disease in humans, yet the pathogenesis remains poorly understood. A hallmark of fatal SFTS cases is the marked depletion of T cells. Previous studies on T cell depletion have predominantly focused on alterations in blood and peripheral lymphoid organs, while the thymus, a critical site for T cell development, has remained largely overlooked. In this study, we employed a lethal murine infection model to investigate the impact of SFTSV on thymic function. Our results revealed that SFTSV infected the thymus and induced severe cortical atrophy in type I interferon receptor-deficient (IFNAR<sup>−/−</sup>) mice, characterized by a dramatic depletion of CD4<sup>+</sup>CD8<sup>+</sup> double-positive (DP) thymocytes. Transcriptomic analysis indicated that thymic damage is likely attributable to impaired thymocyte proliferation and increased apoptosis, which may be a consequence of SFTSV-induced alterations in the thymic microenvironment. We found SFTSV-infected macrophages and dendritic cells in the thymus, which accumulated in the cortex and exhibited elevated secretion of IFN-γ, a cytokine commonly associated with acute thymic atrophy. These results demonstrate thymic atrophy caused by SFTSV infection and suggest potential therapeutic strategies for restoring thymic function and promoting T cell reconstitution.
DOI: 10.6084/m9.figshare.28424474
title: Honey-derived <i>Paenibacillus</i> spp. with potential to affect bee brood development in <i>Apis mellifera</i>: Are they a new threat to honey bees?

description: Honey bees are important pollinators in both agriculture and ecosystems, and their health is essential for sustainable human development. Although only two bacteria, <i>Paenibacillus larvae</i> and <i>Melissococcus plutonius</i>, have been identified as bacterial pathogens in honey bee brood for over 100 years, we found three additional <i>Paenibacillus</i> strains (<i>Paenibacillus</i> sp. J27TS7, <i>Paenibacillus azoreducens</i> J34TS1, and <i>Paenibacillus melissococcoides</i> J46TS7) in honey that harmed honey bee brood development. In particular, <i>Paenibacillus</i> sp. J27TS7 was highly virulent in bee larvae (the median lethal dose [LD<sub>50</sub>] = 12.7 spores/larva) and was comparable to <i>P. larvae</i> (LD<sub>50</sub> = 2.3–11.5 spores/larva). <i>Paenibacillus azoreducens</i> J34TS1 showed the second-highest virulence (LD<sub>50</sub> = 45.9 spores/larva), and <i>P. melissococcoides</i> J46TS7 was the least virulent (LD<sub>50</sub> = 469.0 spores/larva). However, <i>P. melissococcoides</i> was most frequently detected in Japanese honey among the three species, with the highest concentration being 1.8 × 10<sup>6</sup> spores/mL honey, suggesting its wide distribution in Japanese apiaries. The novel pathogenic <i>Paenibacillus</i> species were categorized into the fast killer (<i>Paenibacillus</i> sp. J27TS7), medium-fast killer (<i>P. melissococcoides</i>), and slow killer (<i>P. azoreducens</i>) like <i>P. larvae</i> strains in terms of the time to kill infected brood; however, histopathological and genome analyses indicated that their pathogenic mechanisms were different from those of <i>P. larvae</i> strains. Moreover, <i>P. melissococcoides</i> showed differences in virulence depending on the lineage of the strain. These findings represent the first discovery of honey bee brood pathogens in more than 100 years and indicate the need to look beyond known pathogens for a comprehensive understanding of honey bee diseases.
DOI: 10.6084/m9.figshare.28424474.v1
title: Honey-derived <i>Paenibacillus</i> spp. with potential to affect bee brood development in <i>Apis mellifera</i>: Are they a new threat to honey bees?

description: Honey bees are important pollinators in both agriculture and ecosystems, and their health is essential for sustainable human development. Although only two bacteria, <i>Paenibacillus larvae</i> and <i>Melissococcus plutonius</i>, have been identified as bacterial pathogens in honey bee brood for over 100 years, we found three additional <i>Paenibacillus</i> strains (<i>Paenibacillus</i> sp. J27TS7, <i>Paenibacillus azoreducens</i> J34TS1, and <i>Paenibacillus melissococcoides</i> J46TS7) in honey that harmed honey bee brood development. In particular, <i>Paenibacillus</i> sp. J27TS7 was highly virulent in bee larvae (the median lethal dose [LD<sub>50</sub>] = 12.7 spores/larva) and was comparable to <i>P. larvae</i> (LD<sub>50</sub> = 2.3–11.5 spores/larva). <i>Paenibacillus azoreducens</i> J34TS1 showed the second-highest virulence (LD<sub>50</sub> = 45.9 spores/larva), and <i>P. melissococcoides</i> J46TS7 was the least virulent (LD<sub>50</sub> = 469.0 spores/larva). However, <i>P. melissococcoides</i> was most frequently detected in Japanese honey among the three species, with the highest concentration being 1.8 × 10<sup>6</sup> spores/mL honey, suggesting its wide distribution in Japanese apiaries. The novel pathogenic <i>Paenibacillus</i> species were categorized into the fast killer (<i>Paenibacillus</i> sp. J27TS7), medium-fast killer (<i>P. melissococcoides</i>), and slow killer (<i>P. azoreducens</i>) like <i>P. larvae</i> strains in terms of the time to kill infected brood; however, histopathological and genome analyses indicated that their pathogenic mechanisms were different from those of <i>P. larvae</i> strains. Moreover, <i>P. melissococcoides</i> showed differences in virulence depending on the lineage of the strain. These findings represent the first discovery of honey bee brood pathogens in more than 100 years and indicate the need to look beyond known pathogens for a comprehensive understanding of honey bee diseases.
DOI: 10.6084/m9.figshare.28424474.v2
title: Honey-derived <i>Paenibacillus</i> spp. with potential to affect bee brood development in <i>Apis mellifera</i>: Are they a new threat to honey bees?

description: Honey bees are important pollinators in both agriculture and ecosystems, and their health is essential for sustainable human development. Although only two bacteria, <i>Paenibacillus larvae</i> and <i>Melissococcus plutonius</i>, have been identified as bacterial pathogens in honey bee brood for over 100 years, we found three additional <i>Paenibacillus</i> strains (<i>Paenibacillus</i> sp. J27TS7, <i>Paenibacillus azoreducens</i> J34TS1, and <i>Paenibacillus melissococcoides</i> J46TS7) in honey that harmed honey bee brood development. In particular, <i>Paenibacillus</i> sp. J27TS7 was highly virulent in bee larvae (the median lethal dose [LD<sub>50</sub>] = 12.7 spores/larva) and was comparable to <i>P. larvae</i> (LD<sub>50</sub> = 2.3–11.5 spores/larva). <i>Paenibacillus azoreducens</i> J34TS1 showed the second-highest virulence (LD<sub>50</sub> = 45.9 spores/larva), and <i>P. melissococcoides</i> J46TS7 was the least virulent (LD<sub>50</sub> = 469.0 spores/larva). However, <i>P. melissococcoides</i> was most frequently detected in Japanese honey among the three species, with the highest concentration being 1.8 × 10<sup>6</sup> spores/mL honey, suggesting its wide distribution in Japanese apiaries. The novel pathogenic <i>Paenibacillus</i> species were categorized into the fast killer (<i>Paenibacillus</i> sp. J27TS7), medium-fast killer (<i>P. melissococcoides</i>), and slow killer (<i>P. azoreducens</i>) like <i>P. larvae</i> strains in terms of the time to kill infected brood; however, histopathological and genome analyses indicated that their pathogenic mechanisms were different from those of <i>P. larvae</i> strains. Moreover, <i>P. melissococcoides</i> showed differences in virulence depending on the lineage of the strain. These findings represent the first discovery of honey bee brood pathogens in more than 100 years and indicate the need to look beyond known pathogens for a comprehensive understanding of honey bee diseases.
DOI: 10.6084/m9.figshare.30463567
title: Neutrophil extracellular trap-borne C3-driven endothelial dysfunction in <i>Klebsiella pneumoniae</i> liver abscess

description: <i>Klebsiella pneumoniae</i> (<i>K. pneumoniae</i>) liver abscess (KPLA) is a severe bacterial infection that is frequently complicated by intrahepatic thrombophlebitis and extrahepatic metastatic infections leading to high mortality rates. This study investigates the role of neutrophil extracellular traps (NETs) in endothelial injury and disease progression in KPLA. Our findings reveal that KPLA patients with intrahepatic thrombophlebitis are more prone to developing sepsis and extrahepatic migratory infections. <i>K. pneumoniae</i> induces NET formation via the TLR4-PI3Kα-AKT signaling pathway, and C3 deposition on NETs significantly contributes to endothelial injury. In a KPLA mouse model, increased C3 levels were observed in the liver, with NETs carrying substantial amounts of C3, disrupting the endothelial barrier and exacerbating liver injury. Treatment with the C3 inhibitor AMY-101 reduced C3 deposition on NETs, alleviated endothelial damage, significantly improved survival, and reduced extrahepatic dissemination, inflammatory infiltration, and lung injury while also suppressing systemic inflammation. Our findings underscore the pivotal role of C3 in NET-mediated endothelial damage and the pathogenesis of KPLA. Thus, targeting C3 deposition on NETs may be a promising therapeutic strategy to reduce endothelial injury, thrombosis, and extrahepatic infections in KPLA without compromising neutrophil antimicrobial function.
DOI: 10.6084/m9.figshare.30463567.v1
title: Neutrophil extracellular trap-borne C3-driven endothelial dysfunction in <i>Klebsiella pneumoniae</i> liver abscess

description: <i>Klebsiella pneumoniae</i> (<i>K. pneumoniae</i>) liver abscess (KPLA) is a severe bacterial infection that is frequently complicated by intrahepatic thrombophlebitis and extrahepatic metastatic infections leading to high mortality rates. This study investigates the role of neutrophil extracellular traps (NETs) in endothelial injury and disease progression in KPLA. Our findings reveal that KPLA patients with intrahepatic thrombophlebitis are more prone to developing sepsis and extrahepatic migratory infections. <i>K. pneumoniae</i> induces NET formation via the TLR4-PI3Kα-AKT signaling pathway, and C3 deposition on NETs significantly contributes to endothelial injury. In a KPLA mouse model, increased C3 levels were observed in the liver, with NETs carrying substantial amounts of C3, disrupting the endothelial barrier and exacerbating liver injury. Treatment with the C3 inhibitor AMY-101 reduced C3 deposition on NETs, alleviated endothelial damage, significantly improved survival, and reduced extrahepatic dissemination, inflammatory infiltration, and lung injury while also suppressing systemic inflammation. Our findings underscore the pivotal role of C3 in NET-mediated endothelial damage and the pathogenesis of KPLA. Thus, targeting C3 deposition on NETs may be a promising therapeutic strategy to reduce endothelial injury, thrombosis, and extrahepatic infections in KPLA without compromising neutrophil antimicrobial function.
DOI: 10.7910/dvn/9fo1os
title: SIEX 35443 - Bioprospecção de linhagens de Sorgo e Milho com potencial para resistência ao Meloidogyne javanica

description: Os nematoides constituem um dos principais desafios fitossanitários da agricultura brasileira, exigindo a adoção integrada de diferentes estratégias de manejo para possibilitar a redução efetiva das suas populações no campo. O controle genético é uma das estratégias mais importantes para o manejo dos nematoides, pois pode ser aplicada em grandes extensões de terras e não possuem toxicidade ao meio ambiente e aos seres humanos. Entretanto, para que os produtores tenham acesso aos cultivares altamente produtivos e resistentes aos nematoides, é necessário que as empresas de melhoramento genético direcionem seus esforços no desenvolvimento desses cultivares resistentes. Sendo assim, Parceria Público-Privada (PPP) possibilitam alinhar as necessidades das empresas do setor produtivo em acompanhar os avanços tecnológicos, com as Universidades, que podem apoiar o uso de inovações relevantes para o sistema agrícola. Empresas de melhoramento genético demandam de ensaios de bioprospecção de híbridos de sorgo e milho com potencial resistência a nematoides. Tais ensaios apresentam elevada complexidade e requerem expertise técnica para sua correta execução.
DOI: 10.6084/m9.figshare.30011026
title: Mapping evolutionary paradigm of bovine viral diarrhea virus <i>Npro</i> associated with different organizations of nucleotide

description: The non-structural protein (Npro) of bovine viral diarrhea virus (BVDV) is a crucial virulence factor that impairs the host’s antiviral immune response and facilitates virus production. This study establishes a foundation for understanding how different selective pressures influence the formation of nucleotide pairs, synonymous codon, and context-dependent codon bias (CDCB) in BVDV <i>Npro</i>. BVDV genotype 1 exhibits a greater number of subgenotypes compared to other genotypes, yet its overall nucleotide usage bias in <i>Npro</i> is stronger. Within <i>Npro</i>, certain dinucleotides, specifically CpG and UpA, are notably suppressed, while UpG is selected with high frequency across all genotypes. The BVDV <i>Npro</i> region exhibits a pronounced bias in synonymous codon usage and possesses a genetic capacity to distinguish between genotypes. Unlike the patterns of mononucleotide and synonymous codon usage associated with BVDV genotyping, nucleotide pair usage and CDCB show significant variability due to the high mutation rate in the Npro coding sequence. Despite this variation, both nucleotide architectures demonstrate a unique evolutionary paradigm that goes beyond genotype-specific models. Aside from nucleotide composition constraints imposed by the high mutation rate in the viral genome, natural selective pressures arising from translational selection and host immune response also significantly influence the formation of various nucleotide architectures in the BVDV <i>Npro</i>. By analyzing the genetic characterizations associated with the different nucleotide architectures in the <i>Npro</i>, the diverse repertoire of nucleotide pairs, synonymous codons and CDCB may provide BVDV mutants with ample opportunities for direct adaptation and exaptation, thereby overcoming the robust immune defenses of the host.
DOI: 10.6084/m9.figshare.30011026.v1
title: Mapping evolutionary paradigm of bovine viral diarrhea virus <i>Npro</i> associated with different organizations of nucleotide

description: The non-structural protein (Npro) of bovine viral diarrhea virus (BVDV) is a crucial virulence factor that impairs the host’s antiviral immune response and facilitates virus production. This study establishes a foundation for understanding how different selective pressures influence the formation of nucleotide pairs, synonymous codon, and context-dependent codon bias (CDCB) in BVDV <i>Npro</i>. BVDV genotype 1 exhibits a greater number of subgenotypes compared to other genotypes, yet its overall nucleotide usage bias in <i>Npro</i> is stronger. Within <i>Npro</i>, certain dinucleotides, specifically CpG and UpA, are notably suppressed, while UpG is selected with high frequency across all genotypes. The BVDV <i>Npro</i> region exhibits a pronounced bias in synonymous codon usage and possesses a genetic capacity to distinguish between genotypes. Unlike the patterns of mononucleotide and synonymous codon usage associated with BVDV genotyping, nucleotide pair usage and CDCB show significant variability due to the high mutation rate in the Npro coding sequence. Despite this variation, both nucleotide architectures demonstrate a unique evolutionary paradigm that goes beyond genotype-specific models. Aside from nucleotide composition constraints imposed by the high mutation rate in the viral genome, natural selective pressures arising from translational selection and host immune response also significantly influence the formation of various nucleotide architectures in the BVDV <i>Npro</i>. By analyzing the genetic characterizations associated with the different nucleotide architectures in the <i>Npro</i>, the diverse repertoire of nucleotide pairs, synonymous codons and CDCB may provide BVDV mutants with ample opportunities for direct adaptation and exaptation, thereby overcoming the robust immune defenses of the host.