Abstract
BackgroundRespiratory viral infections can induce different cytokine/chemokine profiles in lung tissues and have a significant influence on patients with asthma. There is little information about the systemic cytokine status in viral respiratory-infected asthmatic patients compared with non-asthmatic patients.ObjectivesThe aim of this study was to determine changes in circulating cytokines (IL-1β, TNF-α, IL-4, IL-5) and chemokines (MCP1: monocyte chemoattractant protein-1 and RANTES: regulated on activation normal T cell expressed and secreted) in patients with an asthmatic versus a non-asthmatic background with respiratory syncytial virus, parainfluenza virus or adenovirus respiratory infection. In addition, human monocyte cultures were incubated with respiratory viruses to determine the cytokine/chemokine profiles.Patients/MethodsPatients with asthmatic (n = 34) and non-asthmatic (n = 18) history and respiratory infections with respiratory syncytial virus, parainfluenza, and adenovirus were studied. Healthy individuals with similar age and sex (n = 10) were used as controls. Cytokine/chemokine content in blood and culture supernatants was determined by ELISA. Monocytes were isolated by Hystopaque gradient and cocultured with each of the above-mentioned viruses.ResultsSimilar increased cytokine concentrations were observed in asthmatic and non-asthmatic patients. However, higher concentrations of chemokines were observed in asthmatic patients. Virus-infected monocyte cultures showed similar cytokine/chemokine profiles to those observed in the patients.ConclusionsCirculating cytokine profiles induced by acute viral lung infection were not related to asthmatic status, except for chemokines that were already increased in the asthmatic status. Monocytes could play an important role in the increased circulating concentration of cytokines found during respiratory viral infections.
Highlights
Viral respiratory tract infections can have profound effects on asthma.[1]
Respiratory viral infections can have a significant influence on asthmatic patients, where viral respiratory infections are found in association with asthma exacerbations.[1,2]
Several cytokines have been described to play an important role in the pathogenesis of asthma: IL-4, IL-5, IL-8, IL-10, IL-12 (p40), IL-13, IL-17, TNFa, IL-1, monocyte chemoattractant protein-1 (MCP-1), RANTES, GM-CSF, eotaxin, and IFNc
Summary
Viral respiratory tract infections can have profound effects on asthma.[1]. Respiratory viral infections can have a significant influence on asthmatic patients, where viral respiratory infections are found in association with asthma exacerbations.[1,2] The infections associated with these wheezing events are multiple and include infections by respiratory syncytial virus (RSV), human rhinovirus, metapneumovirus, parainfluenza, coronavirus, and other viruses. Previous studies have shown differences in the bronchoalveolar lavage cytokine profiles between non-asthmatic and asthmatic patients related to the type of cellular infiltrate observed,[3] suggesting that immune response is related to atopic status. Circulating cytokine response after viral respiratory infection in asthmatic and non-asthmatic status has been little studied. In this regard, circulating blood levels of several cytokines have been reported to be increased during viral respiratory tract infections.[2] These cytokines may represent inflammatory markers with different profiles in asthmatic and nonasthmatic patients. Respiratory viral infections can induce different cytokine/chemokine profiles in lung tissues and have a significant influence on patients with asthma. There is little information about the systemic cytokine status in viral respiratory-infected asthmatic patients compared with non-asthmatic patients
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