Effect of Fungal Exposure on Airway Immunity in Asthma
| dc.contributor.advisor | Chen, Yin | en |
| dc.contributor.author | Huang, Jinjie | |
| dc.contributor.author | Chen, Yin | |
| dc.date.accessioned | 2016-06-22T16:45:58Z | |
| dc.date.available | 2016-06-22T16:45:58Z | |
| dc.date.issued | 2015 | |
| dc.identifier.uri | http://hdl.handle.net/10150/614124 | |
| dc.description | Class of 2015 Abstract | en |
| dc.description.abstract | Objectives: The purpose of this study is to explore potential changes in cytokine and interferon expression during co-infection of rhinovirus and Alternaria. Methods: Alternaria filtrates were used to represent Alternaria spores in real-life. The responses were assessed by production of IL-6, IL-8 and interferon, which were measured by ELISA. mRNA expression was detected by quantitative real-time PCR. For data analysis, a two-sided t-test was performed to compare individual experimental groups. Results: Co-infection of Alternaria and rhinovirus enhanced IL-6 and IL-8 production significantly (p< 0.05). However, Alternaria significantly inhibited production of interferon which would otherwise be induced by rhinovirus. Average interferon-beta (IFN β) production was reduced by about 67%; interferon-lambda (IFN λ) was decrease by about 75%. The differences between treatment and control groups were also statistically significant (p < 0.05). Conclusions: These findings suggested that the Alternaria may cause an imbalanced mucosal antiviral response through inhibiting production of interferon while enhancing production of proinflammatory cytokines. These results indicated that Alternaria may lead to inhibit host innate immunity against virus infection, causing more inflammatory response. | |
| dc.language.iso | en_US | en |
| dc.publisher | The University of Arizona. | en |
| dc.rights | Copyright © is held by the author. | en |
| dc.rights.uri | http://rightsstatements.org/vocab/InC/1.0/ | |
| dc.subject | Fungal Exposure | en |
| dc.subject | Asthma | en |
| dc.subject | Airway | en |
| dc.subject.mesh | Asthma | |
| dc.subject.mesh | Alternaria | |
| dc.title | Effect of Fungal Exposure on Airway Immunity in Asthma | en_US |
| dc.type | text | en |
| dc.type | Electronic Report | en |
| dc.contributor.department | College of Pharmacy, The University of Arizona | en |
| dc.description.collectioninformation | This item is part of the Pharmacy Student Research Projects collection, made available by the College of Pharmacy and the University Libraries at the University of Arizona. For more information about items in this collection, please contact Jennifer Martin, Librarian and Clinical Instructor, Pharmacy Practice and Science, jenmartin@email.arizona.edu. | en |
| html.description.abstract | Objectives: The purpose of this study is to explore potential changes in cytokine and interferon expression during co-infection of rhinovirus and Alternaria. Methods: Alternaria filtrates were used to represent Alternaria spores in real-life. The responses were assessed by production of IL-6, IL-8 and interferon, which were measured by ELISA. mRNA expression was detected by quantitative real-time PCR. For data analysis, a two-sided t-test was performed to compare individual experimental groups. Results: Co-infection of Alternaria and rhinovirus enhanced IL-6 and IL-8 production significantly (p< 0.05). However, Alternaria significantly inhibited production of interferon which would otherwise be induced by rhinovirus. Average interferon-beta (IFN β) production was reduced by about 67%; interferon-lambda (IFN λ) was decrease by about 75%. The differences between treatment and control groups were also statistically significant (p < 0.05). Conclusions: These findings suggested that the Alternaria may cause an imbalanced mucosal antiviral response through inhibiting production of interferon while enhancing production of proinflammatory cytokines. These results indicated that Alternaria may lead to inhibit host innate immunity against virus infection, causing more inflammatory response. |