Home
|
Inbox
|
Search
|
View Abstract
Nasal Fluid IRF7, CXCL9 and CXCL10 Protein Levels Do Not Reflect Altered Nasal Cell mRNA Expression Responses to Different Human Rhinovirus Species in Children with Asthma and Wheezing Exacerbations
Description
.abstract img { width:300px !important; height:auto; display:block; text-align:center; margin-top:10px } .abstract { overflow-x:scroll } .abstract table { width:100%; display:block; border:hidden; border-collapse: collapse; margin-top:10px } .abstract td, th { border-top: 1px solid #ddd; padding: 4px 8px; } .abstract tbody tr:nth-child(even) td { background-color: #efefef; } .abstract a { overflow-wrap: break-word; word-wrap: break-word; }
A2013 - Nasal Fluid IRF7, CXCL9 and CXCL10 Protein Levels Do Not Reflect Altered Nasal Cell mRNA Expression Responses to Different Human Rhinovirus Species in Children with Asthma and Wheezing Exacerbations
Author Block: L. A. Coleman1, L. M. Harris1, S. Khoo2, K. M. Franks2, J. Bizzintino2, F. Prastanti3, J. Everard3, S. Oo1, R. Maciewicz4, C. McCrae4, L. Oberg4, P. N. Le Souef1, A. Bosco5, I. A. Laing2; 1School of Paediatrics and Child Health, University of Western Australia, Perth, Australia, 2School of Biological Sciences, University of Western Australia/Telethon Kids Institute, Perth, Australia, 3School of Biological Sciences, University of Western Australia, Perth, Australia, 4Respiratory, Inflammation and Autoimmunity iMed, AstraZeneca, Gothenburg, Sweden, 5Telethon Kids Institute, Perth, Australia.
Introduction/Hypothesis: Rhinovirus (RV) species C infection is associated with increased severity of acute wheezing and asthma compared with other RV species. RVC utilises a different host cellular receptor to RVA and B, but the mechanisms and pathways activated by RVC and their contribution to the severity of disease are unknown. We have previously identified gene expression differences in nasal cell samples from children with acute asthma and wheezing who were infected with RVC versus RVA. RVC-specific genes included IRF7, whereas CXCL9 and CXCL10 were identified in the RVA-specific response. We hypothesised that protein levels for each of these genes would be different in nasal fluid from children having a respiratory exacerbation and infected with RVC versus RVA.
Methods: Nasal fluid samples were collected from 21 children with RVA and 37 with RVC presenting to our tertiary children’s hospital Emergency Department with acute respiratory illness. CXCL10 and CXCL9 protein were measured as part of a multiplex ELISA (ThermoFisher), whereas IRF7 protein was measured using a single ELISA kit (Cusabio). Urea was measured using a quantitative chromatic assay (BioAssay Systems) and used to standardise the ELISA measurements (presented here as pg protein per μg urea).
Results: CXCL9 levels were not significantly different (Mann-Whitney U=192, p=0.79) between RVA (median 13.27, range 0.34-159.88, n=14) and RVC cases (median 20.66, range 0.37-248.44, n=29). CXCL10 levels were also not significantly different (Mann-Whitney U=234, p=0.90) between RVA (median 0.48, range 0.04-11.41, n=16) and RVC cases (median 0.46, range 0.02-41.19, n=30). IRF7 levels did not differ (Mann-Whitney U=217, p=0.63) between RVA (median 1.88, range 0.15-6.16, n=17) and RVC cases (median 1.62, range 0.19-21.78, n=28).
Conclusion: CXCL9, CXCL10 and IRF7 gene expression in nasal cell samples collected during RVC- vs RVA-induced acute wheezing and/or asthma are different, but this has not translated to alterations in nasal fluid protein levels.
Author Block: L. A. Coleman1, L. M. Harris1, S. Khoo2, K. M. Franks2, J. Bizzintino2, F. Prastanti3, J. Everard3, S. Oo1, R. Maciewicz4, C. McCrae4, L. Oberg4, P. N. Le Souef1, A. Bosco5, I. A. Laing2; 1School of Paediatrics and Child Health, University of Western Australia, Perth, Australia, 2School of Biological Sciences, University of Western Australia/Telethon Kids Institute, Perth, Australia, 3School of Biological Sciences, University of Western Australia, Perth, Australia, 4Respiratory, Inflammation and Autoimmunity iMed, AstraZeneca, Gothenburg, Sweden, 5Telethon Kids Institute, Perth, Australia.
Introduction/Hypothesis: Rhinovirus (RV) species C infection is associated with increased severity of acute wheezing and asthma compared with other RV species. RVC utilises a different host cellular receptor to RVA and B, but the mechanisms and pathways activated by RVC and their contribution to the severity of disease are unknown. We have previously identified gene expression differences in nasal cell samples from children with acute asthma and wheezing who were infected with RVC versus RVA. RVC-specific genes included IRF7, whereas CXCL9 and CXCL10 were identified in the RVA-specific response. We hypothesised that protein levels for each of these genes would be different in nasal fluid from children having a respiratory exacerbation and infected with RVC versus RVA.
Methods: Nasal fluid samples were collected from 21 children with RVA and 37 with RVC presenting to our tertiary children’s hospital Emergency Department with acute respiratory illness. CXCL10 and CXCL9 protein were measured as part of a multiplex ELISA (ThermoFisher), whereas IRF7 protein was measured using a single ELISA kit (Cusabio). Urea was measured using a quantitative chromatic assay (BioAssay Systems) and used to standardise the ELISA measurements (presented here as pg protein per μg urea).
Results: CXCL9 levels were not significantly different (Mann-Whitney U=192, p=0.79) between RVA (median 13.27, range 0.34-159.88, n=14) and RVC cases (median 20.66, range 0.37-248.44, n=29). CXCL10 levels were also not significantly different (Mann-Whitney U=234, p=0.90) between RVA (median 0.48, range 0.04-11.41, n=16) and RVC cases (median 0.46, range 0.02-41.19, n=30). IRF7 levels did not differ (Mann-Whitney U=217, p=0.63) between RVA (median 1.88, range 0.15-6.16, n=17) and RVC cases (median 1.62, range 0.19-21.78, n=28).
Conclusion: CXCL9, CXCL10 and IRF7 gene expression in nasal cell samples collected during RVC- vs RVA-induced acute wheezing and/or asthma are different, but this has not translated to alterations in nasal fluid protein levels.
|
Home
|
Inbox
|
Search
|