Abstract
Airway mucus hypersecretion occurs in response to infection and irritation and poses an important and poorly understood clinical problem. In order to gain insight into its pathogenesis, we have focused on an mRNA encoding the major mucus glycoprotein, mucin. Northern blots showed that mucin mRNA was abundant in the intestine of specific pathogen free rats whereas it was undetectable in the airways of these rats until pathogen-free conditions were suspended and rats acquired Sendai (Parainfluenza I) virus infections. Airway mucin hybridization signals in rats that were both infected with Sendai virus and exposed to SO2 were more intense than those in rats with infection alone. These results suggest that pathogen-and irritant-induced hypersecretion may be partly controlled at the level of mucin mRNA.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Blotting, Northern
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Bronchi / drug effects
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Bronchi / pathology*
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Bronchi / physiology
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Bronchi / ultrastructure
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Intestine, Small / drug effects
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Intestine, Small / pathology*
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Intestine, Small / physiology
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Male
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Microscopy, Electron
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Mucins / genetics*
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Muscle, Smooth / drug effects
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Muscle, Smooth / pathology*
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Muscle, Smooth / physiology
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Mycoplasma Infections / pathology
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Mycoplasma Infections / physiopathology*
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Paramyxoviridae Infections / pathology
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Paramyxoviridae Infections / physiopathology*
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RNA, Messenger / analysis
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RNA, Messenger / genetics*
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RNA, Messenger / metabolism
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Rats
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Rats, Inbred Strains
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Reference Values
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Sulfur Dioxide / toxicity*
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Trachea / drug effects
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Trachea / pathology*
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Trachea / physiology
Substances
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Mucins
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RNA, Messenger
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Sulfur Dioxide