Cytokine responses in primary and secondary respiratory syncytial virus infections

Ugonna, Kelechi; Douros, Konstantinos; Bingle, Colin D.; Everard, Mark L.

doi:10.1038/pr.2016.29

Cited by 15 publications

(13 citation statements)

References 37 publications

(45 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Neutrophil products including myeloperoxidase and neutrophil elastase make significant contributions to mucosal inflammation, increasing airway secretion, coughing, and sneezing (4). Therefore, neutrophils may be critically involved in symptom causation; they also likely contribute to viral transmission by increasing mucus levels, thus enhancing the production of infected respiratory droplets (19).…”

Section: Discussionmentioning

confidence: 99%

Pretreatment with a grape seed proanthocyanidin extract downregulates proinflammatory cytokine expression in airway epithelial cells infected with respiratory syncytial virus

et al. 2019

View full text Add to dashboard Cite

Respiratory syncytial virus (RSV) infections are associated with significant morbidity and mortality. Inflammation is mediated by cytokine secretion from RSV-infected airway epithelial cells. Grape seed proanthocyanidin extract (GSPE) exhibits potent antioxidant capacity, as well as anti-bacterial, anti-viral, anti-carcinogenic, anti-inflammatory and anti-allergic actions. However, few studies have explored the anti-inflammatory effects of GSPE on airway epithelial cells infected with RSV. Airway epithelial A549 cells were pretreated with GSPE and its effects on cytokine production during RSV infection were investigated. A549 cells were infected with RSV, with or without GSPE pretreatment, and cultured for 24, 48 and 72 h. The expression of interleukin (IL)-1β, IL-6 and IL-8, were measured by reverse transcription-quantitative polymerase chain reaction, ELISA and western blotting. RSV infection induced significant increases in proinflammatory cytokine expression. However, GSPE pretreatment decreased the mRNA and protein expression levels of IL-1ß, IL-6 and IL-8. GSPE regulated the immune response by reducing the RSV-induced transcription of proinflammatory cytokines in airway epithelial cells, suggesting that GSPE helps to prevent RSV-induced airway disease.

show abstract

Section: Discussionmentioning

confidence: 99%

Pretreatment with a grape seed proanthocyanidin extract downregulates proinflammatory cytokine expression in airway epithelial cells infected with respiratory syncytial virus

et al. 2019

View full text Add to dashboard Cite

show abstract

“…Studies in humans suggest that RSV can modulate IL-21 secretion. In a cohort study that characterized the primary and secondary cytokine response to RSV infection, IL-21 was not detected in swab nasal secretion samples from infants recruited during two consecutive winters (45). Our data indicated that treatment with IL-21 successfully enhanced humoral responses to RSV, leading to increases in B cell follicles, anti-F (fusion RSV protein) IgG titers, antibody avidity and neutralization capacity.…”

Section: Discussionmentioning

confidence: 74%

RSV Downregulates IL-21/IL-21R On TFH Cells Via PD-L1 Induction In APCs Impairing Protective Humoral Responses

Gassen

Fazolo

Freitas

et al. 2017

Preprint

View full text Add to dashboard Cite

Respiratory syncytial virus (RSV) is the major cause of hospitalization for children under two years of age. RSV vaccines are currently unavailable, and children suffering from multiple reinfections by the same viral strain, fail to develop protective memory responses. Follicular helper T (TFH) cells specialize in providing B cell help to antibody production and affinity maturation, mainly via IL-21 secretion. Although RSV-specific antibodies can be detected upon infection, how they are generated and their relevance against disease protection has not been fully examined. Here, we observed that RSV expands a functionally impaired murine TFH cell population in vitro and vivo, with (which was not peer-reviewed) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity.

show abstract

“…This response was characterized by further increased release of multiple proinflammatory cytokines and chemokines into both epithelial cell supernatant and mouse BAL. The antiviral response to RSV infection has been associated with increases of various cytokines and chemokines ( 43 , 105 , 123 ), some of which have been shown to be associated with more severe disease. For instance, GM-CSF levels are higher in infants with RSV infection requiring ventilation ( 24 ), and the level of CCL-3 (MIP-1α) has a positive correlation with the duration of required supplemental oxygen ( 33 ).…”

Section: Discussionmentioning

confidence: 99%

Titanium dioxide nanoparticles exaggerate respiratory syncytial virus-induced airway epithelial barrier dysfunction

Smallcombe

Harford

Linfield

et al. 2020

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

RSV is the leading cause of lower respiratory tract infections in children worldwide. While most develop a mild, self-limiting illness, some develop severe acute lower respiratory infection and persistent airway disease. Exposure to ambient particulate matter has been linked to asthma, bronchitis, and viral infection in multiple epidemiologic studies. We hypothesized that co-exposure to nanoparticles worsens RSV-induced airway epithelial barrier dysfunction. Bronchial epithelial cells were incubated with titanium dioxide nanoparticles (TiO2-NP) or a combination of TiO2-NP and RSV. Structure and function of epithelial cell barrier were analyzed. Viral titer and the role of reactive oxygen species generation was evaluated. In vivo, mice were intranasally incubated with TiO2-NP, RSV, or a combination. Lungs and bronchoalveolar lavage (BAL) fluid were harvested for analysis of airway inflammation and AJC disruption. RSV-induced AJC disruption was amplified by TiO2-NP. Nanoparticle exposure increased viral infection in epithelial cells. TiO2-NP induced generation of ROS, and pretreatment with antioxidant, N-acetylcysteine, reversed said barrier dysfunction. In vivo, RSV-induced injury and AJC disruption were augmented in the lungs of mice given TiO2-NP. Airway inflammation was exacerbated, as evidenced by increased white blood cell infiltration into the BAL, along with exaggeration of peribronchial inflammation and AJC disruption. These data demonstrate that TiO2-NP exposure exacerbates RSV-induced AJC dysfunction and increases inflammation by mechanisms involving generation of ROS. Further studies are required to determine whether NP exposure plays a role in the health disparities of asthma and other lung diseases, and why some children experience more severe airway disease with RSV infection.

show abstract

Cytokine responses in primary and secondary respiratory syncytial virus infections

Cited by 15 publications

References 37 publications

Pretreatment with a grape seed proanthocyanidin extract downregulates proinflammatory cytokine expression in airway epithelial cells infected with respiratory syncytial virus

Pretreatment with a grape seed proanthocyanidin extract downregulates proinflammatory cytokine expression in airway epithelial cells infected with respiratory syncytial virus

RSV Downregulates IL-21/IL-21R On TFH Cells Via PD-L1 Induction In APCs Impairing Protective Humoral Responses

Titanium dioxide nanoparticles exaggerate respiratory syncytial virus-induced airway epithelial barrier dysfunction

Contact Info

Product

Resources

About