Co-infection and co-pathogenesis of important pathogens in livestock and poultry
Ontology highlight
ABSTRACT:
ORGANISM(S): Sus Scrofa Domesticus
SUBMITTER: 
Huili Liu
PROVIDER: PXD023029 | iProX | Wed Dec 09 00:00:00 GMT 2020
REPOSITORIES: iProX
Similar Datasets
Project description:Pathogens that cause respiratory diseases in poultry are very complicated, and co-infections with multiple pathogens are prevalent. The H9N2 strain of avian influenza virus (AIV) and Escherichia coli (E. coli) are common poultry pathogens that limit the development of the poultry industry. This study aimed to clarify the interaction between these two pathogens and their pathogenic mechanism using a mouse model. Co-infection with H9N2 AIV and E. coli significantly increased the mortality rate of mice compared to single viral or bacterial infections. It also led to the development of more severe lung lesions compared to single viral or bacterial infections. Co-infection further causes a storm of cytokines, which aggravates the host’s disease by regulating the STAT/SOCS and ERK1/2 pathways. Moreover, co-infection mutually benefited the virus and the bacteria by increasing their multiplication rates. Importantly, nitric oxide synthase 2 (NOS2) expression was also significantly enhanced by the co-infection. It played a key role in the rapid proliferation of E. coli in the presence of the coinfecting H9N2 virus. Therefore, our study underscores the role of NOS2 as a determinant for bacteria growth and illustrates its importance as an additional mechanism that enhances influenza virus-bacteria synergy. It further provides a scientific basis for investigating the synergistic infection mechanism between viruses and bacteria.
2021-04-08 | GSE164963 | GEO
Project description:Swine H1N1 influenza virus and streptococcus suis serotype 2 (SS2) are two important contributors to the porcine respiratory disease complex, which have significant economic impacts. Clinically, swine influenza virus and swine streptococcus suis co-infection is common, which will increase the mortality. However, the pathogenesis of the co-infection remains largely unkown. To explore it, gene expression profiling was to performed to detect comprehensive analysis of the global host response induced by H1N1 virus infection alone, SS2 infection alone, H1N1-SS2 co-infection and PBS control.
2016-09-10 | GSE60172 | GEO
Project description:Staphylococcus aureus and Pseudomonas aeruginosa are the most prevalent pathogens that colonize structurally abnormal airways such as those in Cystic Fibrosis (CF) and other chronic obstructive lung diseases. Although these bacteria seem to succeed one another, CF patients acquire coinciding P. aeruginosa and S. aureus pulmonary infections, being co-infection usually associated with decreased lung function and increased frequency of pulmonary exacerbations. In addition, P. aeruginosa and S. aureus pathogens adopt a biofilm mode of growth, which contributes to high tolerance to antibiotic treatment and the recalcitrant nature of these chronic coinfections, leading to significant patient morbidity and mortality. Interactions between P. aeruginosa and S. aureus have been widely studied and it is commonly admitted that P. aeruginosa outcompetes S. aureus, perhaps outcompeting S. aureus for limited nutrients or producing anti-staphylococcal compounds, having S. aureus a minimal contribution to the overall course of the infection. However, the molecular mechanisms behind these interactions are largely unknown. Herein, we decided to characterize the full transcriptome of these dual-species biofilms, to unveil important molecular interactions that can occur between these two bacterial species that are relevant for the pathogenesis of the entire consortia. Our data provide novel insights into the role of interspecies interactions in the pathogenesis of P. aeruginosa and S. aureus co-infections and will contribute to future studies by the research community.
2022-08-03 | GSE195909 | GEO
Project description:Proteomics are widely utilized to investigate growth, breeding, nutrition, and diseases of livestock and poultry. The effects of infections on abundance, post-translational modification, and interactions of host cell proteins have been systematically studied using proteomics methods, such as isoelectric focusing, two-dimensional electrophoresis, and mass spectrometry. The research will increase our understanding of pathogenesis of viral infection and contribute to development of novel anti-viral drugs for the livestock and poultry industries.
2021-05-23 | PXD026209 | iProX
Project description:Epithelial cells are the first line of defense within the lung. Disruption of the epithelial barrier by pathogens enables the systematic dissemination of bacteria or viruses within the host, leading to severe diseases with fatal outcomes. Thus, the lung epithelium can be damaged by seasonal and pandemic influenza A viruses. Influenza A virus infection induced dysregulation of the immune system is beneficial for the dissemination of bacteria to the lower respiratory tract, causing bacterial and viral co-infection. Host cells regulate protein homeostasis and the response to different stimuli, for instance pathogen infections, by post translational modification of proteins. Aside from protein phosphorylation, ubiquitination of proteins is an essential regulatory tool in virtually every cellular process, such as protein homeostasis, the host immune response, cell morphology, and in clearing of cytosolic pathogens. Here, we analyzed the proteome and ubiquitinome of A549 cells in response to Streptococcus pneumoniae D39 Δcps and influenza A virus H1N1 as well as bacterial and viral co-infection. Pneumococcal infection induced alterations in the ubiquitination of proteins involved in the organization of the actin cytoskeleton and Rho GTPases, but had minor effects on the abundance of host proteins. H1N1 infection is reflected by an anti-viral state of A549 cells. Finally, co infection resembled the imprints of both infecting pathogens with a minor increase in the observed alterations in protein and ubiquitination abundance.
2022-02-24 | PXD028465 | Pride
Project description:Pathogens target phytohormone signalling pathways to promote disease. Plants deploy salicylic acid (SA) mediated defences against biotrophs. Pathogens antagonise SA immunity by activating jasmonate signalling, e.g. Pseudomonas syringae pv. tomato DC3000 produces coronatine (COR), a jasmonate (JA) mimic. This study found unexpected dynamics between SA, JA and COR and co-operation between JAZ jasmonate repressor proteins during DC3000 infection. JA did not accumulate until late in the infection process and was higher in leaves challenged with coronatine deficient P. syringae or in the more resistant JA receptor mutant coi1. JAZ regulation was complex and coronatine alone was insufficient to sustainably induce JAZs. RNA was extracted from leaves of wild type Col-0 or the jaz5/10 mutant plants from leaves 6, 8, 12 or 16 hours after challenged with Pseudomonas syringae pv. tomato DC3000.
2015-08-28 | E-GEOD-72461 | biostudies-arrayexpress
Project description:Pathogens target phytohormone signalling pathways to promote disease. Plants deploy salicylic acid (SA) mediated defences against biotrophs. Pathogens antagonise SA immunity by activating jasmonate signalling, e.g. Pseudomonas syringae pv. tomato DC3000 produces coronatine (COR), a jasmonate (JA) mimic. This study found unexpected dynamics between SA, JA and COR and co-operation between JAZ jasmonate repressor proteins during DC3000 infection. JA did not accumulate until late in the infection process and was higher in leaves challenged with coronatine deficient P. syringae or in the more resistant JA receptor mutant coi1. JAZ regulation was complex and coronatine alone was insufficient to sustainably induce JAZs.
2015-08-28 | GSE72461 | GEO
Project description:Mathematical model for HIV, malaria and HIV-malaria co-infection.
2018-05-23 | MODEL1805230001 | BioModels
Project description:Tuberculosis, a chronic granulomatous disease caused by Mycobacterium tuberculosis (Mtb), often becomes exacerbated upon co-infection with other pathogens, yet the underlying immunological mechanisms remain insufficiently understood. Here, mice were initially infected with the hypervirulent Mtb strain K, and later with lymphocytic choriomeningitis virus to investigate the mechanism of severe pulmonary pathology. Virus infection significantly reduced Mtb-specific IFN-g, increased bacterial loads, and aggravated lung inflammation in the lung of Mtb-infected mice, which did not occur in pre-existence of Th1 response by Bacillus Calmette-Guerin vaccination prior to the co-infection. Blockade of type I IFN receptor signaling reinvigorated Mtb-specific IFN-γ response and ameliorated pathogenesis by upregulating pulmonary CXCL9/10 production. Our results demonstrate that virus-induced type I IFN triggers severe immunopathology by deteriorating migration of Mtb-specific IFN-γ-producing T cells, suggesting the balance between type I and type II IFNs determines either control of Mtb or exacerbation of pathology in the lung upon viral infection
2021-02-27 | GSE167650 | GEO