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Altered allergen-induced eosinophil trafficking and physiological dysfunction in airways with preexisting virus-induced injury.

Altered allergen-induced eosinophil trafficking and physiological dysfunction in airways with preexisting virus-induced injury. Research Abstract Details 

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  • Altered allergen-induced eosinophil trafficking and physiological dysfunction in airways with preexisting virus-induced injury. Abstract Text:

    ronald l sorknessRonald L Sorkness,kathryn m herricksKathryn M Herricks,renee j szakalyRenee J Szakaly,robert f lemanskeRobert F Lemanske,louis a rosenthalLouis A Rosenthal,

    Although both asthmatics and allergic rhinitics develop an acute inflammatory response to lower airway allergen challenge, only asthmatics experience airway obstruction resulting from chronic environmental allergen exposure. Hypothesizing that asthmatic airways have an altered response to chronic allergic inflammation, we compared the effects of repeated low-level exposures to inhaled Alternaria extract in sensitized rats with preexisting chronic postbronchiolitis airway dysfunction versus sensitized controls with normal airways. Measurements of air space (bronchoalveolar lavage) inflammatory cells, airway goblet cells, airway wall collagen, airway wall eosinophils, airway alveolar attachments, and pulmonary physiology were conducted after six weekly exposures to aerosolized saline or Alternaria extract. Postbronchiolitis rats, but not those starting with normal airways, had persistent increases in airway wall eosinophils, goblet cell hyperplasia in small airways, and loss of lung elastic recoil after repeated exposure to aerosolized Alternaria extract. Despite having elevated airway wall eosinophils, the postbronchiolitis rats had no eosinophils in bronchoalveolar lavage at 5 days after the last allergen exposure, suggesting altered egression of tissue eosinophils into the air space. In conclusion, rats with preexisting airway pathology had altered eosinophil trafficking and allergen-induced changes in airway epithelium and lung mechanics that were absent in sensitized control rats that had normal airways before the allergen exposures.

    Altered allergen-induced eosinophil trafficking and physiological dysfunction in airways with preexisting virus-induced injury. Publishing Authors By Initials

    rl sorknessRL Sorkness,km herricksKM Herricks,rj szakalyRJ Szakaly,rf lemanskeRF Lemanske,la rosenthalLA Rosenthal,

    For similar viruses: rna viruses: mononegavirales: paramyxoviridae: paramyxovirinae: respirovirus: sendai virus research abstracts see: viruses: rna viruses: mononegavirales: paramyxoviridae: paramyxovirinae: respirovirus: sendai virus research

    PUBMED ID PMID:

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    Altered allergen-induced eosinophil trafficking and physiological dysfunction in airways with preexisting virus-induced injury. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: American journal of physiology. Lung cellular and

    VOLUME: 292

    Page Numbers: L85-91

    Journal Abbreviation: Am. J. Physiol. Lung Cell Mol.

    ISSN: 1040-0605

    DAY: 11

    MONTH: 08

    YEAR: 2006

    Altered allergen-induced eosinophil trafficking and physiological dysfunction in airways with preexisting virus-induced injury. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 100901229

    Altered allergen-induced eosinophil trafficking and physiological dysfunction in airways with preexisting virus-induced injury. Keywords Mesh Terms:

    KEYWORDS: Sendai virus

    MESH TERMS: pathogenicity

    Chemical & Substance for Abstract: Altered allergen-induced eosinophil trafficking and physiological dysfunction in airways with preexisting virus-induced injury. Information

    Substance Name: Allergens

    Registry Number: 0

    Grant and Affiliation Information for Altered allergen-induced eosinophil trafficking and physiological dysfunction in airways with preexisting virus-induced injury.

    AFFILIATION: School of Pharmacy, Department of Medicine, University of Wisconsin at Madison, 777 Highland Ave, Madison, WI 53705, USA. rlsorkne@wisc.edu

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NHLBI

    GRANT: P50 HL 56396

    ACRONYM: HL

    MEDLINETA: Am J Physiol Lung Cell Mol Phy

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