cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.29062731
title: Alterations of the gut commensal <i>Akkermansia muciniphila</i> in patients with COVID-19

description: Dysbiosis of gut microbiota is well established in coronavirus disease 2019 (COVID-19). While studies have attempted to establish a link between the gut commensal <i>Akkermansia muciniphila</i> (<i>A. muciniphila</i>) and COVID-19, the findings have been inconsistent and sometimes controversial. The intestinal microbial abundance information of COVID-19 patients was acquired and analysed from GMrepo database. Subsequently, <i>A. muciniphila’s</i> metabolites, target-genes, and metabolite-target relationships was extracted from GutMGene database. Lastly, coronascape module in Metascape database is used for gene annotation and enrichment analysis in various host cells and tissues after SARS-CoV-2 infection. The results indicated that, in comparison to healthy people, <i>A. muciniphila</i> was significantly elevated in COVID-19 patients. This bacterium was found to be associated with heightened expression of IL-10, TLR2, TLR4, CLGN, CLDN4, TJP2, and TJP3, while concurrently experiencing a reduction in the expression of IL-12A and IL-12B in humans. The regulatory genes of <i>A. muciniphila</i> primarily enhance responses to viruses and cytokines, positively regulate cell migration, and control epithelial cell proliferation. Our study revealed a significant increase in the gut commensal <i>A. muciniphila</i> in COVID-19 patients. This bacterium can modulate host immune responses and may also serve as a probiotic with antiviral properties.
DOI: 10.6084/m9.figshare.29062731.v1
title: Alterations of the gut commensal <i>akkermansia muciniphila</i> in patients with COVID-19

description: Dysbiosis of gut microbiota is well established in coronavirus disease 2019 (COVID-19). While studies have attempted to establish a link between the gut commensal <i>Akkermansia muciniphila</i> (<i>A. muciniphila</i>) and COVID-19, the findings have been inconsistent and sometimes controversial. The intestinal microbial abundance information of COVID-19 patients was acquired and analysed from GMrepo database. Subsequently, <i>A. muciniphila’s</i> metabolites, target-genes, and metabolite-target relationships was extracted from GutMGene database. Lastly, coronascape module in Metascape database is used for gene annotation and enrichment analysis in various host cells and tissues after SARS-CoV-2 infection. The results indicated that, in comparison to the health people, <i>A. muciniphila</i> was significantly elevated in COVID-19 patients. This bacterium was found to be associated with heightened expression of IL-10, TLR2, TLR4, CLGN, CLDN4, TJP2, and TJP3, while concurrently experiencing a reduction in the expression of IL-12A and IL-12B in humans. The regulatory genes of <i>A. muciniphila</i> primarily enhance responses to viruses and cytokines, positively regulate cell migration, and control epithelial cell proliferation. Our study revealed a significant increase in the gut commensal <i>A. muciniphila</i> in COVID-19 patients. This bacterium can modulate host immune responses and may also serve as a probiotic with antiviral properties.
DOI: 10.6084/m9.figshare.29062731.v2
title: Alterations of the gut commensal <i>Akkermansia muciniphila</i> in patients with COVID-19

description: Dysbiosis of gut microbiota is well established in coronavirus disease 2019 (COVID-19). While studies have attempted to establish a link between the gut commensal <i>Akkermansia muciniphila</i> (<i>A. muciniphila</i>) and COVID-19, the findings have been inconsistent and sometimes controversial. The intestinal microbial abundance information of COVID-19 patients was acquired and analysed from GMrepo database. Subsequently, <i>A. muciniphila’s</i> metabolites, target-genes, and metabolite-target relationships was extracted from GutMGene database. Lastly, coronascape module in Metascape database is used for gene annotation and enrichment analysis in various host cells and tissues after SARS-CoV-2 infection. The results indicated that, in comparison to healthy people, <i>A. muciniphila</i> was significantly elevated in COVID-19 patients. This bacterium was found to be associated with heightened expression of IL-10, TLR2, TLR4, CLGN, CLDN4, TJP2, and TJP3, while concurrently experiencing a reduction in the expression of IL-12A and IL-12B in humans. The regulatory genes of <i>A. muciniphila</i> primarily enhance responses to viruses and cytokines, positively regulate cell migration, and control epithelial cell proliferation. Our study revealed a significant increase in the gut commensal <i>A. muciniphila</i> in COVID-19 patients. This bacterium can modulate host immune responses and may also serve as a probiotic with antiviral properties.
DOI: 10.6084/m9.figshare.29556296
title: Outbreak and epidemic of Getah virus infection in swine by virulence-enhanced GIII variant in Henan, central China in 2024

description: The Getah virus (GETV), an emerging mosquito-borne virus, poses a threat to many animal species and probably even humans. Between late July and mid-September, concentrated outbreaks of GETV on pig farms have occurred in multiple regions across Henan, and showed epidemic characteristics. To investigate the genetic characteristics and virulence changes of GETV strains responsible for the GETV epidemic in Henan, a total of 27 GETV strains were isolated from 31 commercial pig farms located in 21 counties. Phylogenetic and sequence alignment analysis results showed that 22 of the isolates formed a distinct cluster within the phylogenetic tree, and the strains in this cluster exhibited 3 amino acid mutations in the non-structural protein nsP3 along with an amino acid mutation in the structural protein E2. Piglet pathogenicity experiments demonstrated that the isolate could induce the characteristic clinical signs of GETV infection in piglets, resulting in 100% mortality. Comparative analysis of pathogenicity in mice showed that the pathogenicity of the GETV GIII variant was significantly enhanced compared with the early isolate. This study is the first to investigate in detail the large-scale, concentrated outbreak and epidemic of GETV infection in pig farms in Henan and confirms that there is a trend of increasing virulence of the GIII variant responsible for this outbreak. The data in this study will contribute to the understanding of the molecular epidemiological characteristics and pathogenicity dynamics of GETV.
DOI: 10.6084/m9.figshare.29556296.v1
title: Outbreak and epidemic of Getah virus infection in swine by virulence-enhanced GIII variant in Henan, central China in 2024

description: The Getah virus (GETV), an emerging mosquito-borne virus, poses a threat to many animal species and probably even humans. Between late July and mid-September, concentrated outbreaks of GETV on pig farms have occurred in multiple regions across Henan, and showed epidemic characteristics. To investigate the genetic characteristics and virulence changes of GETV strains responsible for the GETV epidemic in Henan, a total of 27 GETV strains were isolated from 31 commercial pig farms located in 21 counties. Phylogenetic and sequence alignment analysis results showed that 22 of the isolates formed a distinct cluster within the phylogenetic tree, and the strains in this cluster exhibited 3 amino acid mutations in the non-structural protein nsP3 along with an amino acid mutation in the structural protein E2. Piglet pathogenicity experiments demonstrated that the isolate could induce the characteristic clinical signs of GETV infection in piglets, resulting in 100% mortality. Comparative analysis of pathogenicity in mice showed that the pathogenicity of the GETV GIII variant was significantly enhanced compared with the early isolate. This study is the first to investigate in detail the large-scale, concentrated outbreak and epidemic of GETV infection in pig farms in Henan and confirms that there is a trend of increasing virulence of the GIII variant responsible for this outbreak. The data in this study will contribute to the understanding of the molecular epidemiological characteristics and pathogenicity dynamics of GETV.
DOI: 10.6084/m9.figshare.28956129
title: Interplay of <i>Mycobacterium abscessus</i> and <i>Pseudomonas aeruginosa</i> in experimental models of coinfection: Biofilm dynamics and host immune response

description: The incidence of infection by nontuberculous mycobacteria, mainly <i>Mycobacterium abscessus</i>, is increasing in patients with cystic fibrosis and other chronic pulmonary diseases, leading to an accelerated lung function decline. In most cases, <i>M. abscessus</i> coinfects <i>Pseudomonas aeruginosa</i>, the most common pathogen in these conditions. However, how these two bacterial species interact during infection remains poorly understood. This study explored their behaviour in three relevant pathogenic settings: dual-species biofilm development using a recently developed method to monitor individual species in dual-species biofilms, coinfection in bronchial epithelial cells, and <i>in vivo</i> coinfection in the <i>Galleria mellonella</i> model. The results demonstrated that both species form stable mixed biofilms and reciprocally inhibit single-biofilm progression. Coinfections in bronchial epithelial cells significantly decreased cell viability, whereas in <i>G. mellonella</i>, coinfections induced lower survival rates than individual infections. Analysis of the immune response triggered by each bacterium in bronchial epithelial cell assays and <i>G. mellonella</i> larvae revealed that <i>P. aeruginosa</i> induces the overexpression of proinflammatory and melanization cascade responses, respectively. In contrast, <i>M. abscessus</i> and <i>P. aeruginosa</i> coinfection significantly inhibited the immune response in both models, resulting in worse consequences for the host than those generated by a single <i>P. aeruginosa</i> infection. Overall, this study highlights the novel role of <i>M. abscessus</i> in suppressing immune responses during coinfection with <i>P. aeruginosa</i>, emphasizing the clinical implications for the management of cystic fibrosis and other pulmonary diseases. Understanding these interactions could inform the development of new therapeutic strategies to mitigate the severity of coinfections in vulnerable patients.
DOI: 10.6084/m9.figshare.28956129.v1
title: Interplay of <i>Mycobacterium abscessus</i> and <i>Pseudomonas aeruginosa</i> in experimental models of coinfection: Biofilm dynamics and host immune response

description: The incidence of infection by nontuberculous mycobacteria, mainly <i>Mycobacterium abscessus</i>, is increasing in patients with cystic fibrosis and other chronic pulmonary diseases, leading to an accelerated lung function decline. In most cases, <i>M. abscessus</i> coinfects <i>Pseudomonas aeruginosa</i>, the most common pathogen in these conditions. However, how these two bacterial species interact during infection remains poorly understood. This study explored their behaviour in three relevant pathogenic settings: dual-species biofilm development using a recently developed method to monitor individual species in dual-species biofilms, coinfection in bronchial epithelial cells, and <i>in vivo</i> coinfection in the <i>Galleria mellonella</i> model. The results demonstrated that both species form stable mixed biofilms and reciprocally inhibit single-biofilm progression. Coinfections in bronchial epithelial cells significantly decreased cell viability, whereas in <i>G. mellonella</i>, coinfections induced lower survival rates than individual infections. Analysis of the immune response triggered by each bacterium in bronchial epithelial cell assays and <i>G. mellonella</i> larvae revealed that <i>P. aeruginosa</i> induces the overexpression of proinflammatory and melanization cascade responses, respectively. In contrast, <i>M. abscessus</i> and <i>P. aeruginosa</i> coinfection significantly inhibited the immune response in both models, resulting in worse consequences for the host than those generated by a single <i>P. aeruginosa</i> infection. Overall, this study highlights the novel role of <i>M. abscessus</i> in suppressing immune responses during coinfection with <i>P. aeruginosa</i>, emphasizing the clinical implications for the management of cystic fibrosis and other pulmonary diseases. Understanding these interactions could inform the development of new therapeutic strategies to mitigate the severity of coinfections in vulnerable patients.
DOI: 10.6084/m9.figshare.28013821
title: Human macrophage response to the emerging enteric pathogen <i>Aeromonas veronii</i>: Inflammation, apoptosis, and downregulation of histones

description: This study investigated the pathogenic mechanisms of <i>Aeromonas veronii</i> in macrophages. THP-1 derived macrophages were used as a human macrophage model and were treated with <i>A. veronii</i> strain AS1 isolated from intestinal biopsies of an IBD patient, or <i>Escherichia coli</i> strain K-12. RNA was extracted and subjected to RNA sequencing and comparative transcriptomic analyses. Protein levels of IL-8, IL-1β, IL-18, and TNFα were measured using ELISA, and apoptosis was assessed using caspase 3/7 assays. Both <i>A. veronii</i> AS1 and <i>E. coli</i> K-12 significantly upregulated the expression of many genes involving inflammation. At the protein level, <i>A. veronii</i> AS1 induced significantly higher levels of IL-8, TNFα, mature IL-18 and IL-1β than <i>E. coli</i> K-12, and led to greater elevation of caspase 3/7 activities. Both <i>A. veronii</i> AS1 and <i>E. coli</i> K-12 upregulated the expression of <i>CASP5</i>, but not other caspase genes. <i>A. veronii</i> AS1 significantly downregulated the expression of 20 genes encoding histone proteins that <i>E. coli</i> K-12 did not. The more profound pathogenic effects of <i>A. veronii</i> in inducing inflammation and apoptosis in macrophages than <i>E. coli</i> K-12 are consistent with its role as a human enteric pathogen. The upregulated expression of <i>CASP5</i> and increased release of IL-1β and IL-18 support the role of <i>CASP5</i> in activation of non-canonical inflammasome. The downregulation of histone genes by <i>A. veronii</i> suggests a unique impact on host cell gene expression, which may represent a novel virulence strategy. These findings advance the understanding of pathogenic mechanisms of the emerging human enteric pathogen <i>A. veronii.</i>
DOI: 10.6084/m9.figshare.28013821.v2
title: Human macrophage response to the emerging enteric pathogen <i>Aeromonas veronii</i>: Inflammation, apoptosis, and downregulation of histones

description: This study investigated the pathogenic mechanisms of <i>Aeromonas veronii</i> in macrophages. THP-1 derived macrophages were used as a human macrophage model and were treated with <i>A. veronii</i> strain AS1 isolated from intestinal biopsies of an IBD patient, or <i>Escherichia coli</i> strain K-12. RNA was extracted and subjected to RNA sequencing and comparative transcriptomic analyses. Protein levels of IL-8, IL-1β, IL-18, and TNFα were measured using ELISA, and apoptosis was assessed using caspase 3/7 assays. Both <i>A. veronii</i> AS1 and <i>E. coli</i> K-12 significantly upregulated the expression of many genes involving inflammation. At the protein level, <i>A. veronii</i> AS1 induced significantly higher levels of IL-8, TNFα, mature IL-18 and IL-1β than <i>E. coli</i> K-12, and led to greater elevation of caspase 3/7 activities. Both <i>A. veronii</i> AS1 and <i>E. coli</i> K-12 upregulated the expression of <i>CASP5</i>, but not other caspase genes. <i>A. veronii</i> AS1 significantly downregulated the expression of 20 genes encoding histone proteins that <i>E. coli</i> K-12 did not. The more profound pathogenic effects of <i>A. veronii</i> in inducing inflammation and apoptosis in macrophages than <i>E. coli</i> K-12 are consistent with its role as a human enteric pathogen. The upregulated expression of <i>CASP5</i> and increased release of IL-1β and IL-18 support the role of <i>CASP5</i> in activation of non-canonical inflammasome. The downregulation of histone genes by <i>A. veronii</i> suggests a unique impact on host cell gene expression, which may represent a novel virulence strategy. These findings advance the understanding of pathogenic mechanisms of the emerging human enteric pathogen <i>A. veronii.</i>
DOI: 10.6084/m9.figshare.28912067
title: The inhibitory and anti-inflammatory effects of TMP269 on peste des petits ruminants virus replication

description: Peste des petits ruminants (PPR) is an acute and fatal contagious disease, caused by the PPR virus (PPRV), and is one of the most damaging animal diseases. The replication of many viruses is closely related to the regulation of histone deacetylases (HDACs). TMP269, a selective class IIa HDAC inhibitor, plays an important role in cancer therapy and also modulates viral replication. However, the regulatory effects of TMP269 on PPRV replication remain poorly understood. In this study, we employed western blotting, quantitative Real-time PCR (qRT-PCR), RNA sequencing (RNA-seq), and enzyme-linked immunosorbent assay (ELISA) to evaluate the inhibitory and anti-inflammatory effects of TMP269 on PPRV replication. Western blot analysis showed that TMP269 treatment significantly suppressed PPRV replication in Vero and caprine endometrial epithelial cells (EECs). RNA-seq data revealed that the upregulation of inflammatory response genes induced by PPRV infection was markedly reversed by TMP269. Further, qRT-PCR and ELISA demonstrated that TMP269 decreased the expression of the pro-inflammatory chemokines CCL2, CCL5, CCL7, CXCL8, and cytokine IL-6 during infection, suggesting the vital role of TMP269 in anti-inflammatory processes. Collectively, our findings suggest that the class IIa HDAC inhibitor TMP269 is a promising antiviral agent for PPRV and provides novel insights into the antiviral and anti-inflammatory abilities of TMP269.
DOI: 10.6084/m9.figshare.28912067.v1
title: The inhibitory and anti-inflammatory effects of TMP269 on peste des petits ruminants virus replication

description: Peste des petits ruminants (PPR) is an acute and fatal contagious disease, caused by the PPR virus (PPRV), and is one of the most damaging animal diseases. The replication of many viruses is closely related to the regulation of histone deacetylases (HDACs). TMP269, a selective class IIa HDAC inhibitor, plays an important role in cancer therapy and also modulates viral replication. However, the regulatory effects of TMP269 on PPRV replication remain poorly understood. In this study, we employed western blotting, quantitative Real-time PCR (qRT-PCR), RNA sequencing (RNA-seq), and enzyme-linked immunosorbent assay (ELISA) to evaluate the inhibitory and anti-inflammatory effects of TMP269 on PPRV replication. Western blot analysis showed that TMP269 treatment significantly suppressed PPRV replication in Vero and caprine endometrial epithelial cells (EECs). RNA-seq data revealed that the upregulation of inflammatory response genes induced by PPRV infection was markedly reversed by TMP269. Further, qRT-PCR and ELISA demonstrated that TMP269 decreased the expression of the pro-inflammatory chemokines CCL2, CCL5, CCL7, CXCL8, and cytokine IL-6 during infection, suggesting the vital role of TMP269 in anti-inflammatory processes. Collectively, our findings suggest that the class IIa HDAC inhibitor TMP269 is a promising antiviral agent for PPRV and provides novel insights into the antiviral and anti-inflammatory abilities of TMP269.
DOI: 10.6084/m9.figshare.28013821.v1
title: Human macrophage response to the emerging enteric pathogen <i>aeromonas veronii</i>: Inflammation, apoptosis, and downregulation of histones

description: This study investigated the pathogenic mechanisms of <i>Aeromonas veronii</i> in macrophages. THP-1 derived macrophages were used as a human macrophage model and were treated with <i>A. veronii</i> strain AS1 isolated from intestinal biopsies of an IBD patient, or <i>Escherichia coli</i> strain K-12. RNA was extracted and subjected to RNA sequencing and comparative transcriptomic analyses. Protein levels of IL-8, IL-1β, IL-18, and TNFα were measured using ELISA, and apoptosis was assessed using caspase 3/7 assays. Both <i>A. veronii</i> AS1 and <i>E. coli</i> K-12 significantly upregulated the expression of many genes involving inflammation. At the protein level, <i>A. veronii</i> AS1 induced significantly higher levels of IL-8, TNFα, mature IL-18 and IL-1β than <i>E. coli</i> K-12, and led to greater elevation of caspase 3/7 activities. Both <i>A. veronii</i> AS1 and <i>E. coli</i> K-12 upregulated the expression of <i>CASP5</i>, but not other caspase genes. <i>A. veronii</i> AS1 significantly downregulated the expression of 20 genes encoding histone proteins that <i>E. coli</i> K-12 did not. The more profound pathogenic effects of <i>A. veronii</i> in inducing inflammation and apoptosis in macrophages than <i>E. coli</i> K-12, are consistent with its role as a human enteric pathogen. The upregulated expression of <i>CASP5</i> and increased release of IL-1β and IL-18, support the role of <i>CASP5</i> in activation of non-canonical inflammasome. The downregulation of histone genes by <i>A. veronii</i> suggests a unique impact on host cell gene expression, which may represent a novel virulence strategy. These findings advance the understanding of pathogenic mechanisms of the emerging human enteric pathogen <i>A. veronii.</i>
DOI: 10.6084/m9.figshare.28112041
title: Tanshinone I as a novel therapeutic agent targeting von Willebrand factor-binding protein to mitigate <i>Staphylococcus aureus</i> pathogenicity

description: <i>Staphylococcus aureus</i> (<i>S. aureus</i>) is a prevalent pathogen responsible for a wide range of diseases in humans, contributing to both hospital-acquired and community-acquired infections. The von Willebrand factor-binding protein (vWbp) is pivotal for <i>S. aureus</i> pathogenicity because it induces blood coagulation, thereby facilitating bacterial survival and dissemination within the host. Notably, the absence of vWbp does not hinder <i>S. aureus</i> growth, indicating that vWbp is an attractive target for combating <i>S. aureus</i> infections while mitigating the risk of antibiotic resistance. Our findings revealed that tanshinone I significantly inhibited vWbp-induced coagulation without affecting the proliferation of <i>S. aureus</i>. Hemolysis assays confirmed the biocompatibility of tanshinone I, while Western blot analysis, fluorescence quenching, and thermal shift assays (TSAs) demonstrated that tanshinone I does not alter vWbp expression but directly binds to the protein. Molecular docking studies elucidated the interaction mechanism, identifying ARG-479 and GLN-484 as critical residues for tanshinone I binding. Furthermore, <i>in vivo</i> studies demonstrated that tanshinone I reduces lung tissue damage in mice infected with <i>S. aureus</i>, thereby increasing survival rates. Additionally, tanshinone I was tested in greater wax moth larvae and showed similar protective effects. In conclusion, tanshinone I effectively inhibits vWbp, reducing the virulence of <i>S. aureus</i>. This study underscores the potential of tanshinone I as a therapeutic agent against <i>S. aureus</i> infections, offering a novel strategy to combat bacterial infections while decreasing the critical issue of antibiotic resistance.