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Departments of
* Geriatric and Respiratory Medicine and
Cellular Pharmacology, Tohoku University School of Medicine, and
Virus Center, Clinical Research Division, Sendai National Hospital, Sendai, Japan;
Department of Pulmonary Medicine, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Japan; and
¶ Clinical Research Program in Allergic Diseases, Division of Allergic Diseases and Internal Medicine, Mayo Clinic, Rochester, MN 55905
To understand the biochemical events that occur in the airways
after rhinovirus (RV) infection, we developed for the first time a
model in which the cell lines from human mast cells (HMC-1) and
basophils (KU812) can be infected with RV14, a major group RV. Viral
infection was confirmed by demonstrating that viral titers in culture
supernatants, and RV RNA increased with time. RV14 infection alone and
a combination of PMA plus calcium ionophore A23187, did not increase
histamine production by these cells, although IgE plus anti-IgE
increased the histamine production. However, histamine content in the
supernatants increased in response to PMA plus A23187, or IgE plus
anti-IgE after RV14 infection. PMA plus A23187 or IgE plus
anti-IgE induced the production of IL-8 and GM-CSF in supernatants
of HMC-1 cells and IL-4 and IL-6 in supernatants of KU812 cells. RV14
infection further increased the production of the cytokines, whereas
RV14 infection alone did not alter the production of the cytokines by
these cells. An Ab to ICAM-1 inhibited RV14 infection of the cells and
decreased the production of cytokines and histamine after RV14
infection. RV14 infection enhanced the increases in intracellular
calcium concentration and activation of NF-
B by PMA plus A23187 in
the cells. These findings suggest that RV14 infection may prime the
cytokine and histamine production from mast cells and basophils and may
cause airway inflammation in asthma.
This article has been cited by other articles:
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  A. Masuda, A. Nakamura, T. Maeda, Y. Sakamoto, and T. Takai Cis binding between inhibitory receptors and MHC class I can regulate mast cell activation J. Exp. Med., April 16, 2007; 204(4): 907 - 920. [Abstract] [Full Text] [PDF]
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 X. Wang, C. Lau, S. Wiehler, A. Pow, T. Mazzulli, C. Gutierrez, D. Proud, and C.-W. Chow Syk Is Downstream of Intercellular Adhesion Molecule-1 and Mediates Human Rhinovirus Activation of p38 MAPK in Airway Epithelial Cells J. Immunol., November 15, 2006; 177(10): 6859 - 6870. [Abstract] [Full Text] [PDF]
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