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A role for inflammatory mediators in airway hyper-responsiveness
C L Armour1, J L Black, P R Johnson
1Department of Pharmacology, University of Sydney, N.S.W., Australia.
Progress in Clinical and Biological Research
|January 1, 1988
Summary
Prostaglandin F2 alpha (PGF2 alpha) increases airway contraction, potentially via thromboxane A2 (TxA2). This finding may explain airway hyperresponsiveness in asthma, as these mediators are released by inflammatory cells.
Area of Science:
- Respiratory Medicine
- Pharmacology
- Immunology
Background:
- Prostaglandin F2 alpha (PGF2 alpha) is known to potentiate airway contraction.
- Previous studies suggested thromboxane A2 (TxA2) as a potential mediator for this response.
- Airway hyperresponsiveness observed in vivo has not been replicated in vitro.
Purpose of the Study:
- To investigate the mechanism of PGF2 alpha-induced airway potentiation.
- To determine the site of action for PGF2 alpha in airway smooth muscle.
- To explore the role of TxA2 in mediating airway hyperresponsiveness.
Main Methods:
- In vitro studies of airway contraction.
- Localization of PGF2 alpha's site of action relative to parasympathetic ganglia.
- Administration of PGF2 alpha and a TxA2 analogue to assess airway sensitivity.
Main Results:
- PGF2 alpha potentiates airway contraction in vitro.
- The effect of PGF2 alpha is localized distal to parasympathetic ganglia and is specific, as PGD2 had no similar effect.
- TxA2 or a TxA2 analogue increased airway sensitivity in vitro.
- Mediators like TxA2, with short half-lives, may explain the difference between in vivo and in vitro hyperresponsiveness.
Conclusions:
- PGF2 alpha potentiates airway contraction, likely mediated by TxA2.
- These mediators may contribute to the increased airway responsiveness seen in asthma.
- The short half-life and inflammatory cell origin of TxA2 could explain its role in vivo hyperresponsiveness.