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Late-phase reaction in asthma: basic mechanisms

A Pradalier1

  • 1Centre d'Allergie, Hôpital Rothschild, Paris, France.

International Archives of Allergy and Immunology
|January 1, 1993
PubMed
Summary
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Pathologie-biologie·2005

Allergens trigger airway inflammation via mast cells and T cells, leading to increased eosinophils and neutrophils during the late-phase reaction (LPR) in asthma. This cellular influx correlates with airway hyperresponsiveness.

Area of Science:

  • Immunology
  • Pulmonology
  • Cell Biology

Background:

  • Allergens initiate early-phase reactions mediated by mast cells, releasing inflammatory mediators.
  • These mediators recruit and activate eosinophils and neutrophils, crucial in the late-phase reaction (LPR).

Purpose of the Study:

  • To elucidate the cellular and molecular mechanisms underlying allergen-induced late-phase reactions in asthma.
  • To investigate the role of inflammatory cell infiltration and mediator release in airway hyperresponsiveness.

Main Methods:

  • Analysis of broncho-alveolar lavage (BAL) fluid from asthmatic patients exhibiting LPR.
  • Quantification of inflammatory cell counts (eosinophils, neutrophils) and mediator levels.
  • Assessment of airway sensitivity to methacholine and histamine.

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Main Results:

  • Elevated eosinophil and neutrophil numbers in BAL fluid 4 hours post-allergen challenge in LPR-positive asthmatics.
  • Increased airway sensitivity to methacholine and histamine correlated with eosinophil and cationic protein levels in BAL.
  • Evidence of epithelial damage due to eosinophil cationic proteins.

Conclusions:

  • The late-phase reaction in asthma involves significant infiltration of eosinophils and neutrophils.
  • Inflammatory cell mediators, including cationic proteins, contribute to airway hyperresponsiveness and epithelial damage.
  • Basophils, lymphocytes, and released lymphokines like interleukin-5 play roles in modulating the inflammatory cascade.