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Molecular basis for selective eosinophil trafficking in asthma: A multistep paradigm
1Division of Respiratory Medicine, Leicester University Medical School, Leicester, United Kingdom.
The Journal of Allergy and Clinical Immunology
|November 7, 1999
Summary
Asthma involves a significant increase in eosinophils due to multiple molecular events. Targeting key pathways like interleukin-5 (IL-5) can inhibit eosinophil recruitment in asthma.
Area of Science:
- Immunology
- Pulmonology
- Cell Biology
Background:
- Asthma is defined by a substantial increase in eosinophils within the bronchial mucosa compared to neutrophils.
- This eosinophilia results from a complex, multi-step process rather than a single molecular trigger.
Purpose of the Study:
- To elucidate the sequential molecular events driving eosinophil recruitment in asthma.
- To identify potential therapeutic targets for inhibiting eosinophil migration and accumulation.
Main Methods:
- The study outlines a multistep model of eosinophil recruitment.
- Key molecular interactions and signaling pathways, including cytokine and chemokine involvement, are described.
Main Results:
- Eosinophil increase is driven by sequential 4-fold enhancements in migration.
- Specific steps include bone marrow effects (IL-5 mediated), enhanced adhesion (P-selectin/PSGL-1, VLA-4/VCAM-1), chemotaxis (CC chemokines), and prolonged survival (IL-5).
- Allergen-specific T(H)2 lymphocytes orchestrate these events via IL-5, IL-4, and IL-13.
Conclusions:
- The multistep nature of eosinophil recruitment presents multiple targets for therapeutic intervention.
- Antagonists targeting IL-5, VLA-4, P-selectin glycoprotein ligand 1 (PSGL-1), CCR3, IL-4, and IL-13 show potential for inhibiting eosinophil recruitment in asthma.