Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.697010
Title: The influence of biological response modifiers on cytokine production induced by respiratory syncytial virus infected airway epithelial cells
Author: Gould, Melanie Emma Louise
Awarding Body: University of Leicester
Current Institution: University of Leicester
Date of Award: 2001
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Abstract:
The incidence of asthma is on the increase in industrialised countries. Many researchers have reported that respiratory viruses, such as respiratory syncytial virus (RSV), can induce exacerbations in asthma. However, indoor contaminants, including lipopolysaccharide (LPS), -glucan and house dust mite (HDM) allergens, have been identified as respiratory irritants or aeroallergens. No data has been previously published which examines any combination of the above in respect to their combined effect on airway epithelium. Airway epithelial cells (BEAS-2B) were infected with RSV alone, or after pre-treatment with LPS, -glucan or HDM. Investigations included: i. an immunoplaque assay for the detection of the RSV glycoprotein (G-protein), ii. IL-6, IL-8 and RANTES mRNA expression by RT-PCR and iii. IL-8 and RANTES protein release in culture supernatants by ELISA. Infection with RSV induced a time and multiplicity of infection dependent increase in IL-6, IL-8 and RANTES mRNA and IL-8 and RANTES protein release. Pre-treatment of BEAS-2B cells with LPS decreased RSV infectivity and RSV-induced IL-8 and RANTES protein release (p<0.01). RSV infection appeared to be altered by pre-treatment with -glucan and HDM, but this data was not definitive. Indoor contaminants, especially LPS, have been shown by others to show an ability to alter RSV infection and, as a consequence, the immune response that RSV infection initiates. The data on the ability that LPS can decrease RSV infection might be useful in combating the disease. A greater understanding of the properties of indoor contaminants and their interaction with the epithelium during infection may result in an increased knowledge of the immune responses initiated by airway epithelial cells, and help provide an insight into the mechanisms behind asthma.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.697010  DOI: Not available
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