The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Interactions between Innate Antiviral and Atopic Immunoinflammatory Pathways Precipitate and Sustain Asthma Exacerbations in Children
Abstract
Severe asthma exacerbations in children requiring hospitalization are typically associated with viral infection and occur almost exclusively among atopics, but the significance of these comorbidities is unknown. We hypothesized that underlying interactions between immunoinflammatory pathways related to responses to aeroallergen and virus are involved, and that evidence of these interactions is detectable in circulating cells during exacerbations. To address this hypothesis we used a genomics-based approach involving profiling of PBMC subpopulations collected during exacerbation vs convalescence by microarray and flow cytometry. We demonstrate that circulating T cells manifest the postactivated “exhausted” phenotype during exacerbations, whereas monocyte/dendritic cell populations display up-regulated CCR2 expression accompanied by phenotypic changes that have strong potential for enhancing local inflammation after their recruitment to the atopic lung. Notably, up-regulation of FcεR1, which is known to markedly amplify capacity for allergen uptake/presentation to Th2 effector cells via IgE-mediated allergen capture, and secondarily programming of IL-4/IL-13-dependent IL-13R+ alternatively activated macrophages that have been demonstrated in experimental settings to be a potent source of autocrine IL-13 production. We additionally show that this disease-associated activation profile can be reproduced in vitro by cytokine exposure of atopic monocytes, and furthermore that IFN-α can exert both positive and negative roles in the process. Our findings suggest that respiratory viral infection in atopic children may initiate an atopy-dependent cascade that amplifies and sustains airway inflammation initiated by innate antiviral immunity via harnessing underlying atopy-associated mechanisms. These interactions may account for the unique susceptibility of atopics to severe viral-induced asthma exacerbations.
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Cites
Subramanian, A., Tamayo, P., Mootha, V. K., Mukherjee, S., Ebert, B. L., Gillette, M. A., Paulovich, A., Pomeroy, S. L., Golub, T. R., Lander, E. S., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0506580102 · Cited by 53,625
Smyth, G. K. (2004) · Statistical Applications in Genetics and Molecular Biology · doi:10.2202/1544-6115.1027 · Cited by 11,829
Alternative activation of macrophages
Gordon, S. (2003) · Nature Reviews Immunology · doi:10.1038/nri978 · Cited by 6,189
Molecular Signature of CD8+ T Cell Exhaustion during Chronic Viral Infection
Wherry, E. J., Ha, S.-J., Kaech, S. M., Haining, W. N., Sarkar, S., Kalia, V., Subramaniam, S., Blattman, J. N., Barber, D. L., & Ahmed, R. (2007) · Immunity · doi:10.1016/j.immuni.2007.09.006 · Cited by 2,103
Microarray data analysis: from disarray to consolidation and consensus
Allison, D. B., Cui, X., Page, G. P., & Sabripour, M. (2006) · Nature Reviews Genetics · doi:10.1038/nrg1749 · Cited by 1,339 · cited 1×
“This pooling strategy using independent RNA pools was employed to minimize the effect of biological variation between different individuals in producing outliers and bias in the results (26, 27) The pooled RNA samples were labeled and hybridized to Affymetrix U133 Plus 2.”
MethodKim, E. Y., Battaile, J. T., Patel, A. C., You, Y., Agapov, E., Grayson, M. H., Benoit, L. A., Byers, D. E., Alevy, Y., Tucker, J., et al. (2008) · Nature Medicine · doi:10.1038/nm1770 · Cited by 523
Holt, P. G., Haining, S., Nelson, D. J., & Sedgwick, J. D. (1994) · The Journal of Immunology · doi:10.4049/jimmunol.153.1.256 · Cited by 347
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Cited by
Comparison of childhood wheezing phenotypes in 2 birth cohorts: ALSPAC and PIAMA
Savenije, O. E., Granell, R., Caudri, D., Koppelman, G. H., Smit, H. A., Wijga, A., de Jongste, J. C., Brunekreef, B., Sterne, J. A., Postma, D. S., et al. (2011) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2011.02.002 · Cited by 351
Holt, P. G., & Sly, P. D. (2012) · Nature Medicine · doi:10.1038/nm.2768 · Cited by 296
Self-citationEpigenetics and Allergy: from Basic Mechanisms to Clinical Applications
Potaczek, D. P., Harb, H., Michel, S., Alhamwe, B. A., Renz, H., & Tost, J. (2017) · Epigenomics · doi:10.2217/epi-2016-0162 · Cited by 284
Structural Basis of Signaling Blockade by Anti-IL-13 Antibody Lebrikizumab
Ultsch, M., Bevers, J., Nakamura, G., Vandlen, R., Kelley, R. F., Wu, L. C., & Eigenbrot, C. (2013) · Journal of Molecular Biology · doi:10.1016/j.jmb.2013.01.024 · Cited by 174
Macrophage heterogeneity in respiratory diseases
Boorsma, C. E., Draijer, C., & Melgert, B. N. (2013) · Mediators of Inflammation · doi:10.1155/2013/769214 · Cited by 126
Metadata
- Authors
- Subrata, L. S., Bizzintino, J., Mamessier, E., Bosco, A., McKenna, K. L., Wikström, M. E., Goldblatt, J., Sly, P. D., Hales, B. J., Thomas, W. R., Laing, I. A., LeSouëf, P. N., & Holt, P. G.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2009-08
- Volume
- 183
- Issue
- 4
- Pages
- 2793-2800
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1525354362
- Cited by
- 212
- References
- 7
- FWCI
- 15.94
- Type
- journal article
- Language
- en
- Open access
- closed
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- Subrata, L. S., Bizzintino, J., Mamessier, E., Bosco, A., McKenna, K. L., Wikström, M. E., Goldblatt, J., Sly, P. D., Hales, B. J., Thomas, W. R., Laing, I. A., LeSouëf, P. N., & Holt, P. G. (2009). Interactions between Innate Antiviral and Atopic Immunoinflammatory Pathways Precipitate and Sustain Asthma Exacerbations in Children. The Journal of Immunology. https://doi.org/10.4049/jimmunol.0900695
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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