The DOI matches its Crossref record; 22 of the 22 references it cites were found in a registry or an index.
A common cold virus, rhinovirus 16, potentiates airway inflammation after segmental antigen bronchoprovocation in allergic subjects.
Open accessAbstract
Many patients with asthma have increased wheezing with colds. We hypothesized that rhinovirus colds might increase asthma by augmenting airway allergic responses (histamine release and eosinophil influx) after antigen challenge. Seven allergic rhinitis patients and five normal volunteers were infected with rhinovirus type 16 (RV16) and evaluated by segmental bronchoprovocation and bronchoalveolar lavage. Segmental challenge with saline and antigen was performed 1 mo before infection, during the acute infection, and 1 mo after infection. Lavage was performed immediately and 48 h after antigen challenge. Data were analyzed by two-way analysis of variance, and a P value of < or = 0.05 was considered to be significant. All volunteers inoculated with RV16 developed an acute respiratory infection. BAL fluid obtained from allergic rhinitis subjects during the acute viral infection, and 1 mo after infection, showed the following significant RV16-associated changes after antigen challenge: (a) an enhanced release of histamine immediately after local antigen challenge; (b) persistent histamine leak 48 h afterwards; and (c) a greater recruitment of eosinophils to the airway 48 h after challenge. These changes were not seen in non-allergic volunteers infected with RV16 and challenged with antigen, nor in allergic volunteers repetitively challenged with antigen but not infected with RV16, nor in RV16 infected allergic volunteers sham challenged with saline. We conclude that rhinovirus upper respiratory infection significantly augments immediate and late allergic responses in the airways of allergic individuals after local antigen challenge. These data suggest that one mechanism of increased asthma during a cold is an accentuation of allergic responses in the airway which may then contribute to bronchial inflammation.
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Self-citationLiu, M. C., Hubbard, W. C., Proud, D. M., Stealey, B. A., Galli, S. J., Kagey‐Sobotka, A., Bleecker, E. R., & Lichtenstein, L. M. (1991) · American Review of Respiratory Disease · doi:10.1164/ajrccm/144.1.51 · Cited by 378
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Cited by
Allergic Rhinitis and Its Impact on Asthma
Bousquet, J., van Cauwenberge, P., & Khaltaev, N. (2001) · Journal of Allergy and Clinical Immunology · doi:10.1067/mai.2001.118891 · Cited by 3,588
Asthma: From Bronchoconstriction to Airways Inflammation and Remodeling
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Self-citationRhinovirus illnesses during infancy predict subsequent childhood wheezing
Lemanske, R. F., Jackson, D. J., Gangnon, R. E., Evans, M. D., Li, Z., Shult, P. A., Kirk, C. J., Reisdorf, E., Roberg, K. A., Anderson, E. L., et al. (2005) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2005.06.024 · Cited by 735
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T H 2 and T H 17 inflammatory pathways are reciprocally regulated in asthma
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Metadata
- Authors
- Calhoun, W. J., Dick, E. C., Schwartz, L. B., & Busse, W. W.
- Venue
- Journal of Clinical Investigation
- Published
- 1994-12-01
- Volume
- 94
- Issue
- 6
- Pages
- 2200-2208
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2054090763
- Cited by
- 300
- References
- 22
- FWCI
- 6.62
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Calhoun, W. J., Dick, E. C., Schwartz, L. B., & Busse, W. W. (1994). A common cold virus, rhinovirus 16, potentiates airway inflammation after segmental antigen bronchoprovocation in allergic subjects. Journal of Clinical Investigation. https://doi.org/10.1172/jci117581
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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