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Mechanisms of decrease in cytoplasmic motility of alveolar macrophages during immediate asthmatic response in dogs
M Yamaya1, K Zayasu, K Sekizawa
1First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
The American Journal of Physiology
|April 1, 1990
Summary
Immediate asthmatic responses involve changes in alveolar macrophage cytoplasmic motility. Prostaglandin E2 (PGE2) and platelet-activating factor (PAF) altered macrophage relaxation rates, suggesting their role in asthma pathogenesis.
Area of Science:
- Pulmonary immunology
- Cellular physiology
- Pharmacology
Background:
- Alveolar macrophages (AM) play a role in asthma.
- Cytoplasmic motility (CM) of AM is a key cellular function.
- Measuring CM in vivo is challenging.
Purpose of the Study:
- To investigate AM cytoplasmic motility during immediate asthmatic responses.
- To correlate AM motility with respiratory changes after antigen inhalation.
- To identify mediators influencing AM motility.
Main Methods:
- In vivo measurement of remanent filed strength (RFS) in dogs after Ascaris suum-antigen (AA) inhalation to assess AM CM via particle relaxation rate (lambda 0).
- In vitro assessment of lambda 0 in AM exposed to various inflammatory mediators.
- Pharmacological inhibition of prostaglandin synthesis using indomethacin and diclofenac sodium.
Main Results:
- AA inhalation significantly decreased lambda 0 in responder dogs, indicating reduced AM CM.
- Indomethacin and diclofenac sodium inhibited the AA-induced decrease in lambda 0 but not the increase in respiratory resistance.
- In vitro, prostaglandin E1 and E2 dose-dependently decreased lambda 0, while histamine and platelet-activating factor increased it.
Conclusions:
- AM cytoplasmic motility is altered during immediate asthmatic responses.
- Prostaglandins, particularly PGE2, may modulate AM motility during asthma.
- Nonsteroidal anti-inflammatory drugs (NSAIDs) may affect AM function independently of bronchoconstriction.