Apoptosis, Toll-like, RIG-I-like and NOD-like receptors are pathways jointly induced by diverse respiratory bacterial and viral pathogens
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE88825 | GEO | 2017/03/01
SECONDARY ACCESSION(S): PRJNA348741
REPOSITORIES: GEO
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Project description:With annually 2.56 million deaths worldwide, pneumonia is one of the leading causes of death. Most frequent causative pathogens are Streptococcus pneumoniae and influenza A virus. Lately, the interaction between pathogens, the host and its microbiome gained more attention. A healthy microbiome is known to enhance the immune response towards pathogens, however, our knowledge on how infections affect the microbiome is still scarce. In this study, a meta-omics approach was used to investigate the impact of S. pneumoniae and influenza A virus infection on structure and function of the respiratory and gastrointestinal microbiomes of mice. In particular, the taxonomic composition of the respiratory microbiome was less affected by bacterial colonization and viral infection compared to S. pneumoniae infection. Pneumococcal pneumonia led to reduction of bacterial families and lower diversity in the respiratory microbiome, whereas diversity/richness was unaffected following H1N1 infection. Within the gastrointestinal microbiome we found exclusive changes in structure and function depending on the pneumonia inducing pathogen. Exemplarily, increased abundance of Akkermansiaceae and Spirochaetaceae, as well as decreased amounts of Clostridiaceae in response to S. pneumoniae infection, while increased presence of Enterococcaceae and Staphylococcaceae was specific for viral-induced pneumonia. Investigation of the intestinal microbiomes functional composition revealed reduced expression of flagellin and rubrerythrin and increased levels of ATPase during pneumococcal infection, while increased amounts of acetyl-CoA acetyltransferase and, enoyl-CoA transferase were unique after H1N1 infection. The identification of specific taxonomical and functional profiles during infection with a respective pathogen could deliver new insights in the role of the microbiome during disease and be beneficial for discrimination of pneumococcal- or viral-induced pneumonia.
2023-03-24 | PXD036129 | Pride
Project description:With annually 2.56 million deaths worldwide, pneumonia is one of the leading causes of death. Most frequent causative pathogens are Streptococcus pneumoniae and influenza A virus. Lately, the interaction between pathogens, the host and its microbiome gained more attention. A healthy microbiome is known to enhance the immune response towards pathogens, however, our knowledge on how infections affect the microbiome is still scarce. In this study, a meta-omics approach was used to investigate the impact of S. pneumoniae and influenza A virus infection on structure and function of the respiratory and gastrointestinal microbiomes of mice. In particular, the taxonomic composition of the respiratory microbiome was less affected by bacterial colonization and viral infection compared to S. pneumoniae infection. Pneumococcal pneumonia led to reduction of bacterial families and lower diversity in the respiratory microbiome, whereas diversity/richness was unaffected following H1N1 infection. Within the gastrointestinal microbiome we found exclusive changes in structure and function depending on the pneumonia inducing pathogen. Exemplarily, increased abundance of Akkermansiaceae and Spirochaetaceae, as well as decreased amounts of Clostridiaceae in response to S. pneumoniae infection, while increased presence of Enterococcaceae and Staphylococcaceae was specific for viral-induced pneumonia. Investigation of the intestinal microbiomes functional composition revealed reduced expression of flagellin and rubrerythrin and increased levels of ATPase during pneumococcal infection, while increased amounts of acetyl-CoA acetyltransferase and, enoyl-CoA transferase were unique after H1N1 infection. The identification of specific taxonomical and functional profiles during infection with a respective pathogen could deliver new insights in the role of the microbiome during disease and be beneficial for discrimination of pneumococcal- or viral-induced pneumonia.
2023-03-24 | PXD036115 | Pride
Project description:With annually 2.56 million deaths worldwide, pneumonia is one of the leading causes of death. Most frequent causative pathogens are Streptococcus pneumoniae and influenza A virus. Lately, the interaction between pathogens, the host and its microbiome gained more attention. A healthy microbiome is known to enhance the immune response towards pathogens, however, our knowledge on how infections affect the microbiome is still scarce. In this study, a meta-omics approach was used to investigate the impact of S. pneumoniae and influenza A virus infection on structure and function of the respiratory and gastrointestinal microbiomes of mice. In particular, the taxonomic composition of the respiratory microbiome was less affected by bacterial colonization and viral infection compared to S. pneumoniae infection. Pneumococcal pneumonia led to reduction of bacterial families and lower diversity in the respiratory microbiome, whereas diversity/richness was unaffected following H1N1 infection. Within the gastrointestinal microbiome we found exclusive changes in structure and function depending on the pneumonia inducing pathogen. Exemplarily, increased abundance of Akkermansiaceae and Spirochaetaceae, as well as decreased amounts of Clostridiaceae in response to S. pneumoniae infection, while increased presence of Enterococcaceae and Staphylococcaceae was specific for viral-induced pneumonia. Investigation of the intestinal microbiomes functional composition revealed reduced expression of flagellin and rubrerythrin and increased levels of ATPase during pneumococcal infection, while increased amounts of acetyl-CoA acetyltransferase and, enoyl-CoA transferase were unique after H1N1 infection. The identification of specific taxonomical and functional profiles during infection with a respective pathogen could deliver new insights in the role of the microbiome during disease and be beneficial for discrimination of pneumococcal- or viral-induced pneumonia.
2023-03-24 | PXD036014 | Pride
Project description:With annually 2.56 million deaths worldwide, pneumonia is one of the leading causes of death. Most frequent causative pathogens are Streptococcus pneumoniae and influenza A virus. Lately, the interaction between pathogens, the host and its microbiome gained more attention. A healthy microbiome is known to enhance the immune response towards pathogens, however, our knowledge on how infections affect the microbiome is still scarce. In this study, a meta-omics approach was used to investigate the impact of S. pneumoniae and influenza A virus infection on structure and function of the respiratory and gastrointestinal microbiomes of mice. In particular, the taxonomic composition of the respiratory microbiome was less affected by bacterial colonization and viral infection compared to S. pneumoniae infection. Pneumococcal pneumonia led to reduction of bacterial families and lower diversity in the respiratory microbiome, whereas diversity/richness was unaffected following H1N1 infection. Within the gastrointestinal microbiome we found exclusive changes in structure and function depending on the pneumonia inducing pathogen. Exemplarily, increased abundance of Akkermansiaceae and Spirochaetaceae, as well as decreased amounts of Clostridiaceae in response to S. pneumoniae infection, while increased presence of Enterococcaceae and Staphylococcaceae was specific for viral-induced pneumonia. Investigation of the intestinal microbiomes functional composition revealed reduced expression of flagellin and rubrerythrin and increased levels of ATPase during pneumococcal infection, while increased amounts of acetyl-CoA acetyltransferase and, enoyl-CoA transferase were unique after H1N1 infection. The identification of specific taxonomical and functional profiles during infection with a respective pathogen could deliver new insights in the role of the microbiome during disease and be beneficial for discrimination of pneumococcal- or viral-induced pneumonia.
2023-03-24 | PXD036279 | Pride
Project description:Rationale: Respiratory syncytial virus (RSV) and Streptococcus pneumoniae are major respiratory pathogens. Co-infection with RSV and S. pneumoniae is associated with severe and often fatal pneumonia but the molecular basis for this remains unclear. Objectives: To determine if interaction between RSV and pneumococci enhances pneumococcal virulence. Methods: We used confocal microscopy and western blot to identify the receptors involved in direct binding of RSV and pneumococci, the effects of which were studied in both in vivo and in vitro models of infection. Human ciliated respiratory epithelial cell cultures were infected with RSV for 72h and then challenged with pneumococci. Pneumococci were collected after 2h exposure and changes in gene expression determined using qRT-PCR. Results: Following incubation with RSV or purified G protein, pneumococci demonstrated a significant increase in the inflammatory response and bacterial adherence to human ciliated epithelial cultures and markedly increased virulence in a pneumonia model in mice. This was associated with extensive changes in the pneumococcal transcriptome and significant upregulation in the expression of key pneumococcal virulence genes, including the gene for the pneumococcal toxin, pneumolysin. We show that mechanistically this is due to RSV G glycoprotein binding penicillin binding protein 1a. Conclusion: The direct interaction between a respiratory virus protein and the pneumococcus resulting in increased bacterial virulence and worsening disease outcome is a new paradigm in respiratory infection. Comparison of the Streptococcus pneumoniae D39 RSV treated compared to BSA Treated in BEBM medium One condition design comparision of two strains including a dye swap
2014-06-21 | E-GEOD-58425 | biostudies-arrayexpress
Project description:Rationale: Respiratory syncytial virus (RSV) and Streptococcus pneumoniae are major respiratory pathogens. Co-infection with RSV and S. pneumoniae is associated with severe and often fatal pneumonia but the molecular basis for this remains unclear. Objectives: To determine if interaction between RSV and pneumococci enhances pneumococcal virulence. Methods: We used confocal microscopy and western blot to identify the receptors involved in direct binding of RSV and pneumococci, the effects of which were studied in both in vivo and in vitro models of infection. Human ciliated respiratory epithelial cell cultures were infected with RSV for 72h and then challenged with pneumococci. Pneumococci were collected after 2h exposure and changes in gene expression determined using qRT-PCR. Results: Following incubation with RSV or purified G protein, pneumococci demonstrated a significant increase in the inflammatory response and bacterial adherence to human ciliated epithelial cultures and markedly increased virulence in a pneumonia model in mice. This was associated with extensive changes in the pneumococcal transcriptome and significant upregulation in the expression of key pneumococcal virulence genes, including the gene for the pneumococcal toxin, pneumolysin. We show that mechanistically this is due to RSV G glycoprotein binding penicillin binding protein 1a. Conclusion: The direct interaction between a respiratory virus protein and the pneumococcus resulting in increased bacterial virulence and worsening disease outcome is a new paradigm in respiratory infection. Comparison of the Streptococcus pneumoniae D39 Protein P treated compared to Protein GTreated in BEBM medium One condition design comparision of two strains including a dye swap
2014-06-21 | E-GEOD-58424 | biostudies-arrayexpress
Project description:Viral respiratory infections significantly affect young children, particularly extremely premature infants, resulting in high hospitalization rates and increased health-care burdens. Despite posing substantial health risks, airway immune responses in early life remain largely unexplored. Nasal epithelial cells, the primary defense against respiratory infections, are vital for understanding nasal immune responses and serve as a promising target for uncovering underlying molecular and cellular mechanisms. Using a trans-well pseudostratified nasal epithelial cell system, we examined age-dependent developmental differences and antiviral responses to influenza A and respiratory syncytial virus through systems biology approaches. Our studies revealed differences in innate-receptor repertoires, distinct developmental pathways, and differentially connected antiviral network circuits between neonatal and adult nasal epithelial cells. Consensus network analysis identified unique and shared cellular networks for influenza A and respiratory syncytial virus, emphasizing highly relevant virus-specific pathways. This research highlights the importance of nasal epithelial cells in innate antiviral immune responses and offers novel insights that should enable a deeper understanding of age-related differences in nasal epithelial cell immunity following respiratory virus infections.
2024-11-06 | PXD042209 | Pride
Project description:Viral infections facilitate bacterial trafficking to the lower respiratory tract resulting in bacterial viral co infections. Bacterial dissemination to the lower respiratory tract is enhanced by influenza A virus induced epithelial cell damage and dysregulation of immune responses. Epithelial cells act as the first line of defense and detect pathogens by a high variety of pattern recognition receptors. The post translational modification ubiquitin is involved in almost every cellular process. Moreover, ubiquitination contributes to the regulation of host immune responses, influenza A virus uncoating and transport within host cells. We applied proteomics with a special focus on ubiquitination to assess the impact of single bacterial and viral as well as bacterial viral co-infections on bronchial epithelial cells. We used Tandem Ubiquitin Binding Entities to enrich polyubiquitinated proteins and assess changes in the ubiquitinome. Infecting 16HBE cells with Streptococcus pyogenes led to an increased abundance of proteins related to mitochondrial translation and energy metabolism in proteome and ubiquitinome. In contrast, influenza A virus infection mainly altered the ubiquitinome. Co-infections had no additional impact on protein abundances or affected pathways. Changes in protein abundance and enriched pathways were assigned to imprints of both infecting pathogens.
2022-02-24 | PXD025146 | Pride
Project description:Rationale: Lower respiratory tract infections continue to exact unacceptable worldwide mortality, often because the infecting pathogen cannot be identified. The respiratory epithelia provide protection from pneumonias through organism-specific generation of antimicrobial products, offering potential insight into the identity of infecting pathogens. Objective: This study assesses the capacity of the host gene expression response to infection to predict lower respiratory pathogens without reliance on culture data. Methods: Mice were inhalationally challenged with S. pneumoniae, P. aeruginosa, A. fumigatus or PBS prior to whole genome gene expression microarray analysis of their pulmonary parenchyma. Characteristic gene expression patterns for each condition were identified, allowing the derivation of prediction rules for each pathogen. After confirming the predictive capacity of gene expression data in blinded challenges, a computerized algorithm was devised to predict the infectious conditions of subsequent subjects. Measurements and Main Results: We observed robust, pathogen-specific gene expression patterns as early as 2 h after infection. We were able to develop a predictive model that used a limited number of specifically regulated transcripts to discriminate perfectly among infecting pathogens in the training data. Validation trials using an algorithmic decision tree revealed 94.4% diagnostic accuracy when discerning the presence of bacterial infection. The model subsequently differentiated between bacterial pathogens with 71.4% accuracy and between non-bacterial conditions with 70.0% accuracy, both far exceeding the expected diagnostic yield of standard culture-based bronchoscopy with bronchoalveolar lavage. Conclusions: These data substantiate the specificity of the pulmonary innate immune response and support the feasibility of a gene expression-based clinical tool for pneumonia diagnosis. Keywords: pathogen- and time-dependent host lung gene expression changes in pneumonia Mouse lungs were removed 6 h after challenge with P. aeruginosa, S. pneumoniae, A. fumigatus or sham (PBS), RNA was collected from leukoreduced lung homogenates, then cRNA was amplified and hybridized to Illumina Sentrix mouse-6 gene expression arrays v1.1. Gene expression data was analyzed to determine if there were distinct patterns of host trasnscription that corresponded with a specific infection.
2009-04-29 | E-GEOD-15869 | biostudies-arrayexpress
Project description:Background: Swine influenza is a highly contagious viral infection in pigs affecting the respiratory tract that can have significant economic impacts. Streptococcus suis serotype 2 is one of the most important post-weaning bacterial pathogens in swine causing different infections, including pneumonia. Both pathogens are important contributors to the porcine respiratory disease complex. Outbreaks of swine influenza virus with a significant level of co-infections due to S. suis have lately been reported. In order to analyze a global response to the dual infection, we carried out a comprehensive gene expression profiling using a microarray approach to study the swine tracheal epithelial (NPTr) cell response to a co-infection with H1N1 swine influenza virus (swH1N1) and S. suis serotype 2. Results: Gene clustering showed that the swH1N1 and swH1N1/S. suis infections modified the expression of genes in a similar manner. Additionally, infection of NPTr cells by S. suis alone did not result in many differentially expressed genes compared to mock-infected cells. However, some important genes coding for inflammatory mediators, such as chemokines, interleukins, cell adhesion molecules and eicosanoids, were significantly upregulated in the presence of both pathogens comparing to infection with each pathogen taken individually. This synergy may also be the consequence of an increased adhesion/invasion of epithelial cells previously infected by swH1N1, as recently reported. Conclusion: In a co-infection situation, influenza virus would replicate in the respiratory epithelium inducing an inflammatory infiltrate comprised of mononuclear cells and neutrophils. Despite that these cells are unable to phagocyte and kill S. suis, they are highly activated by this pathogen. S. suis is not considered a primary pulmonary pathogen, but an exacerbated production of pro-inflammatory mediators during a co-infection with influenza virus may be of critical importance in the pathogenesis and outcome of this respiratory disease complex. Total RNA obtained from NPTr cells infected with S. suis, H1N1, or S. suis & H1N1. Four replicates in both groups.
2014-05-01 | E-GEOD-52172 | biostudies-arrayexpress