Experimental rhinovirus 16 infection potentiates histamine release after antigen bronchoprovocation in allergic subjects

William Calhoun, C. A. Swenson, E. C. Dick, L. B. Schwartz, R. F. Lemanske, W. W. Busse

Research output: Contribution to journalArticle

107 Scopus citations

Abstract

Viral respiratory infections exacerbate asthma in many patients. We hypothesized that one mechanism by which this effect occurs may include potentiated or altered mediator release by mast cells and/or basophils to favor the development of late-phase asthmatic reactions (LAR). Therefore, we studied eight subjects with allergic rhinitis before and during an experimentally induced rhinovirus 16 (RV16) infection. We determined levels of plasma histamine and tryptase, and we observed the associated patterns of airway obstruction that developed following inhaled antigen challenge. Bronchial responsiveness to histamine, methacholine, and antigen were all significantly increased during the RV16 illness. Further, the incidence of LAR was significantly higher (five of eight) during the infection than before (one of eight; p = 0.014). In addition, in those patients whose pattern of response following antigen challenge converted from an immediate response only before infection to a dual response (immediate + late phase) during infection, plasma histamine concentrations after challenge were significantly greater than in those whose pattern of response did not change. We conclude that one mechanism by which RV16 infection increases the likelihood of LAR could include enhanced mediator release from pulmonary mast cells or from circulating or recruited basophils.

Original languageEnglish (US)
Pages (from-to)1267-1273
Number of pages7
JournalAmerican Review of Respiratory Disease
Volume144
Issue number6
StatePublished - 1991
Externally publishedYes

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ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

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