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Major and Minor Group Human Rhinovirus Response in Human Macrophages

ABSTRACT: Major- and minor-group rhinoviruses enter their host by binding to the cell surface molecules ICAM-1 and LDL-R, respectively, which are present on both macrophages and epithelial cells. Although epithelial cells are the primary site of productive HRV infection, previous studies have implicated macrophages in establishing the cytokine dysregulation that occurs during rhinovirus-induced asthma exacerbations. Even though major- and minor-group rhinoviruses are nearly genetically identical, these viruses do not replicate with equal success in monocyte-lineage cell lines. In human primary macrophages, differential mitochondrial activity and signaling pathway activation was observed between major- and minor-group rhinovirus upon initial HRV binding, indicating discordant receptor-dependent response to these rhinovirus types. As well, variances in phosphorylation of kinases (p38, JNK, ERK5) and transcription factors (ATF-2, CREB, CEBP-alpha) were observed between the major- and minor- group HRV treatments. The difference between major- and minor- group HRV activation of signaling pathways was confirmed through RNA-sequencing and observation of differential production of the asthma-relevant cytokines CCL20, CCL2, and IL-10. This is the first report of genetically similar viruses eliciting dissimilar cytokine release, transcription factor phosphorylation, and MAPK activation from macrophages. These results suggest that receptor dependence plays a role in establishing the inflammatory microenvironment initiated in part by monocytic-lineage cells in the human airway upon exposure to rhinovirus. RNA sequencing of monocyte-derived macrophages after mock infection or infection by HRV16 or HRV1A

ORGANISM(S): Homo sapiens

SUBMITTER: Michal Mokry

PROVIDER: E-GEOD-55271 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Major and Minor Group Human Rhinovirus Response in Human Macrophages

Project description:Major- and minor-group rhinoviruses enter their host by binding to the cell surface molecules ICAM-1 and LDL-R, respectively, which are present on both macrophages and epithelial cells. Although epithelial cells are the primary site of productive HRV infection, previous studies have implicated macrophages in establishing the cytokine dysregulation that occurs during rhinovirus-induced asthma exacerbations. Even though major- and minor-group rhinoviruses are nearly genetically identical, these viruses do not replicate with equal success in monocyte-lineage cell lines. In human primary macrophages, differential mitochondrial activity and signaling pathway activation was observed between major- and minor-group rhinovirus upon initial HRV binding, indicating discordant receptor-dependent response to these rhinovirus types. As well, variances in phosphorylation of kinases (p38, JNK, ERK5) and transcription factors (ATF-2, CREB, CEBP-alpha) were observed between the major- and minor- group HRV treatments. The difference between major- and minor- group HRV activation of signaling pathways was confirmed through RNA-sequencing and observation of differential production of the asthma-relevant cytokines CCL20, CCL2, and IL-10. This is the first report of genetically similar viruses eliciting dissimilar cytokine release, transcription factor phosphorylation, and MAPK activation from macrophages. These results suggest that receptor dependence plays a role in establishing the inflammatory microenvironment initiated in part by monocytic-lineage cells in the human airway upon exposure to rhinovirus.

2014-03-14 | GSE55271 | GEO

Transcription profiling of human bronchial epithelial cells from normal and asthmatic individuals to investigate rhinovirus-induced modulation of gene expression

Project description:Human Rhinovirus (HRV) infection can trigger exacerbations of asthma. Understanding of the mechanisms provoking airway inflammation and remodeling in asthma, as well as the pathogenic mechanisms of HRV infection and its association with asthma exacerbations, may offer significant opportunities for improved disease management. Genome-wide expression analysis of HRV type 1A-infected primary bronchial epithelial (PBE) cells from normal and asthmatic donors was performed to determine whether asthma is associated with a unique pattern of gene expression after HRV infection in vitro. Experiment Overall Design: Frozen stocks of human PBE cells obtained from the bronchial brushings of six normal and five asthmatic individuals were grown in vitro in Bronchial Epithelial Growth Media (BEGM, Lonza). Subconfluent monolayers of PBE cells were infected with purified and concentrated minor group HRV serotype 1A at multiplicity of infection of 10 plaque forming units (pfu) per cell or mock-infected with growth media alone. Cells were lysed 16 hours post infection (p.i.) and isolated total RNAs were analyzed using the Human Genome U133 Plus 2.0 GeneChip arrays (Affymetrix, Santa Clara, CA).

2008-11-13 | E-GEOD-13396 | biostudies-arrayexpress

Rhinovirus-induced modulation of gene expression in bronchial epithelial cells from subjects with asthma

2008-11-01 | GSE13396 | GEO

Homo sapiens

Project description:Major and Minor Group Human Rhinovirus Response in Human Macrophages

| PRJNA239024 | ENA

IL-33 induces an antiviral signature in mast cells but enhances their permissiveness for human rhinovirus infection

Project description:Mast cells (MCs) are classically associated with allergic asthma but their role in antiviral immunity is unclear. Human rhinoviruses (HRVs) are a major cause of asthma exacerbations and can infect and replicate within MCs. The primary site of HRV infection is the airway epithelium and MCs localise to this site with increasing asthma severity. The asthma susceptibility gene, IL-33, encodes an epithelial-derived cytokine released following HRV infection but its impact on MC antiviral responses has yet to be determined. In this study we investigated the global response of LAD2 MCs to IL-33 stimulation using RNA sequencing and identified genes involved in antiviral immunity. In spite of this, IL-33 treatment increased permissiveness of MCs to HRV16 infection which, from the RNA-Seq data, we attributed to upregulation of ICAM1. Flow cytometric analysis confirmed an IL-33-dependent increase in ICAM1 surface expression as well as LDLR, the receptors used by major and minor group HRVs for cellular entry. Neutralisation of ICAM1 reduced the IL-33-dependent enhancement in HRV16 replication and release in both LAD2 MCs and cord blood derived MCs. These findings demonstrate that although IL-33 induces an antiviral signature in MCs, it also upregulates the receptors for HRV entry to enhance infection. This highlights the potential for a gene-environment interaction involving IL33 and HRV in MCs to contribute to virus-induced asthma exacerbations.

2022-11-01 | GSE216269 | GEO

Distinct peripheral blood mononuclear cells transcriptional modules in the response to human respiratory syncytial virus or human rhinovirus in hospitalized infants with bronchiolitis

Project description:Human respiratory syncytial virus (HRSV) is the main cause of bronchiolitis during the first year of life, but other viruses such as rhinovirus also occur and are clinically indistinguishable. In hospitalized infants with bronchiolitis, the analysis of the peripheral blood mononuclear cells (PBMC) gene expression might be useful for identification the etiologies caused by HRSV and human rhinovirus (HRV) and to the development of future tests, as well as to elucidate the pathogenic mechanisms triggered by different viral agents and new therapeutic possibilities. In this study, we conducted a comparative global gene expression analysis of infants with acute viral bronchiolitis infected by HRSV (HRSV group) or HRV (HRV group).

2019-03-19 | GSE124124 | GEO

Phenotypic responses of differentiated asthmatic human airway epithelial cultures to rhinovirus

Project description:We report the application of RNA sequencing technology for high-throughput profiling of gene expression responses to human rhinovirus infection at 24 hours in air-liquid interface human airway epithelial cell cultures derived from 6 asthmatic and 6 non-asthmatic donors. RNA-seq analysis identified sets of genes associated with asthma specific viral responses. These genes are related to inflammatory pathways, epithelial remodeling and cilium assembly and function, including those described previously (e.g. CCL5, CXCL10 and CX3CL1), and novel ones that were identified for the first time in this study (e.g. CCRL1, CDHR3). We concluded that air liquid interface cultured human airway epithelial cells challenged with live HRV are a useful in vitro model for the study of rhinovirus induced asthma exacerbation, given that our findings are consistent with clinical data sets. Furthermore, our data suggest that abnormal airway epithelial structure and inflammatory signaling are important contributors to viral induced asthma exacerbation. Differentiated air-liquid interface cultured human airway epithelial cell mRNA profiles from 6 asthmatic and 6 non-asthmatic donors after 24 hour treatment with either HRV or vehicle control were generated by deep sequencing, using Illumina HiSeq 2000.

2015-03-01 | E-GEOD-61141 | biostudies-arrayexpress

Transcription profiling of human nasal epithelium from subjects infected with HRV-16 rhinovirus vs sham infected

Project description:This study provides a comprehensive evaluation of changes in gene expression during rhinovirus infections in vivo. Subjects were experimentally infected with HRV-16 rhinovirus (RV16) or sham infected (control). Nasal epithelial scrapings collected and processed for microarray analysis. Only subjects exhibiting rhinovirus infection were analyzed. Experiment Overall Design: Randomized, parallel group study. A total of 31 subjects was analyzed: 15 infected and 16 controls. Nasal scapings were taken 14 days prior to infection (d14) and 8 hours (d0) and 2 days (d2) after infection. For each collection, alternating nostrils were used (e.g. -14d = left, 8hr = right, 2d=left) and subjects were randomized for collection (e.g. LRL, RLR).

2008-06-12 | E-GEOD-11348 | biostudies-arrayexpress

Phenotypic responses of differentiated asthmatic human airway epithelial cultures to rhinovirus

2015-03-01 | GSE61141 | GEO

Rhinovirus infection results in stronger and more persistent genomic dysregulation: evidence for altered innate immune response in asthmatics at baseline, early in infection, and during convalescence

Project description:Background: Rhinovirus (HRV) is associated with the large majority of virus-induced asthma exacerbations in children and young adults, but the mechanisms remain poorly defined. Methods: Asthmatics and non-asthmatic controls were inoculated with HRV-A16, and nasal epithelial samples were obtained 7 days before, 36 hours after, and 7 days after viral inoculation. RNA was extracted and subjected to RNA-seq analysis. Results: At baseline, 57 genes were differentially expressed between asthmatics and controls, and the asthmatics had decreased expression of viral replication inhibitors and increased expression of genes involved in inflammation. At 36 hours (before the emergence of peak symptoms), 1329 genes were significantly altered from baseline in the asthmatics compared to 62 genes in the controls. At this time point, asthmatics lacked an increase in IL-10 signaling observed in the controls. At 7 days following HRV inoculation, 222 genes were significantly dysregulated in the asthmatics, whereas only 4 genes were dysregulated among controls. At this time point, the controls but not asthmatics demonstrated upregulation of SPINK5. Conclusions: As judged by the magnitude and persistence of dysregulated genes, asthmatics have a substantially different host response to HRV-A16 infection compared with non-asthmatic controls. Gene expression differences illuminate biologically plausible mechanisms that contribute to a better understanding of the pathogenesis of HRV-induced asthma exacerbations.

2017-05-26 | GSE97668 | GEO

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