ArticleClinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology2010
Human monocytic cells direct the robust release of CXCL10 by bronchial epithelial cells during rhinovirus infection.
Article in Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 52 citations in OpenAlex.
- The rhinovirus puzzle: Linking virus and host factors to childhood asthma.The Journal of allergy and clinical immunology · 2026Review
- Protective effect of interferon type I on barrier function of human airway epithelium during rhinovirus infections in vitro.Scientific reports · 2024Article
- IL-1β-Induced CXCL10 Expression in THP-1 Monocytic Cells Involves the JNK/c-Jun and NF-κB-Mediated Signaling.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Rhinovirus C15 Attenuates Relaxation and cAMP Production in Human Airways and Smooth Muscle.American journal of respiratory cell and molecular biology · 2023Article
- In Vitro Effects of 5-Lipoxygenase Pathway Inhibition on Rhinovirus-Associated Bronchial Epithelial Inflammation.Pulmonary therapy · 2021Article
- The novel immunomodulatory biologic LMWF5A for pharmacological attenuation of the "cytokine storm" in COVID-19 patients: a hypothesis.Patient safety in surgery · 2020Article
- Human Rhinovirus Infections in Hematopoietic Cell Transplant Recipients: Risk Score for Progression to Lower Respiratory Tract Infection.Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation · 2019Article
- Respiratory epithelial cells as master communicators during viral infections.Current clinical microbiology reports · 2019Article
- DUSP10 Negatively Regulates the Inflammatory Response to Rhinovirus through Interleukin-1β Signaling.Journal of virology · 2019Article
- Asthmatic Bronchial Smooth Muscle Increases CCL5-Dependent Monocyte Migration in Response to Rhinovirus-Infected Epithelium.Frontiers in immunology · 2019Article
- Modulation of airway hyperresponsiveness by rhinovirus exposure.Respiratory research · 2018Review
- HRV16 Impairs Macrophages Cytokine Response to a Secondary Bacterial Trigger.Frontiers in immunology · 2018Article
- Severe asthma in humans and mouse model suggests a CXCL10 signature underlies corticosteroid-resistant Th1 bias.JCI insight · 2017Article
- Association of ORMDL3 with rhinovirus-induced endoplasmic reticulum stress and type I Interferon responses in human leucocytes.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2017Article
- Toll-like Receptor 7 Is Reduced in Severe Asthma and Linked to an Altered MicroRNA Profile.American journal of respiratory and critical care medicine · 2016Article
- House Dust Mite Allergens and the Induction of Monocyte Interleukin 1β Production That Triggers an IκBζ-Dependent Granulocyte Macrophage Colony-Stimulating Factor Release from Human Lung Epithelial Cells.American journal of respiratory cell and molecular biology · 2015Article
- CCL20 and Beta-Defensin 2 Production by Human Lung Epithelial Cells and Macrophages in Response to Brucella abortus Infection.PloS one · 2015Article
- LPS modulates rhinovirus-induced chemokine secretion in monocytes and macrophages.American journal of respiratory cell and molecular biology · 2014Article
- Simvastatin attenuates rhinovirus-induced interferon and CXCL10 secretion from monocytic cells in vitro.Journal of leukocyte biology · 2014Article
- Allergen challenge in vivo alters rhinovirus-induced chemokine secretion from human airway macrophages.The Journal of allergy and clinical immunology · 2014Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundHuman rhinovirus (HRV) infections are a major cause of exacerbations in chronic respiratory conditions such as asthma and chronic obstructive pulmonary disease, but HRV-induced immune responses of the lower airway are poorly understood. Earlier work examining cytokine release following HRV infection has focused on epithelial cells because they serve as the principal site of viral replication, and internalization and replication of viral RNA appear necessary for epithelial cell mediator release. However, during HRV infection, only a small proportion of epithelial cells become infected. As HRV-induced cytokine levels in vivo are markedly elevated, this observation suggests that other mechanisms independent of direct viral infection may induce epithelial cell cytokine release.
objectiveOur aim was to test for the importance of interactions between human bronchial epithelial cells (HBECs) and monocytic cells in the control of mediator release during HRV exposure.
methodsIn vitro models of HRV serotype-16 (HRV16) infection of primary HBECs and human monocytic cells, in mono or co-culture, were used. We assessed HRV16-induced CXCL10 and CCL2 protein release via ELISA.
resultsCo-culture of human monocytic and bronchial epithelial cells promoted a synergistic augmentation of CXCL10 and CCL2 protein release following HRV16 challenge. Transfer of conditioned media from HRV16-treated monocytic cells to epithelial cultures induced a robust release of CXCL10 by the epithelial cells. This effect was greatly attenuated by type I IFN receptor blocking antibodies, and could be recapitulated by IFN-alpha addition.
conclusionsOur data indicate that epithelial CXCL10 release during HRV infection is augmented by a monocytic cell-dependent mechanism involving type I IFN(s). Our findings support a key role for monocytic cells in the amplification of epithelial cell chemokine production during HRV infection, and help to explain how an inflammatory milieu is created in the lower airways even in the absence of extensive viral replication and epithelial infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.