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Published on: July 10, 2018
Pulmonary edema measured by MRI correlates with late-phase response to allergen challenge
Rhys L Evans1, Kumar K Changani, Sarah Hotee
11Division of Pharmacology, Cardiff School of Pharmacy & Pharmaceutical Science, Cardiff University, Cardiff, United Kingdom.
Purpose:
Asthma is associated with reversible airway obstruction, leucocyte infiltration, airways hyperresponsiveness (AHR), and airways remodeling. Fluid accumulation causes pulmonary edema contributing to airways obstruction. We examined the temporal relationship between the late asthmatic response (LAR) following allergen challenge of sensitized guinea-pigs and pulmonary edema measured by magnetic resonance imaging (MRI).
Materials And Methods:
Ovalbumin (OVA) sensitized guinea-pigs received either a single OVA inhalation (acute) or nine OVA inhalations at 48 h intervals (chronic). Airways obstruction was measured as specific airways conductance (sG(aw)) by whole body plethysmography. AHR to inhaled histamine and bronchoalveolar lavage for leucocyte counts were measured 24 h after a single or the final chronic ovalbumin challenges. MRI was performed at intervals after OVA challenge and high-intensity edemic signals were quantified.
Results:
Ovalbumin caused early bronchoconstriction, followed at 7 h by an LAR and at 24 h AHR and leucocyte influx. The bright-intensity MRI edema signal, peaking at 7 h, was significantly (P < .05) greater after chronic (9.0 ± 0.7 × 10(3) mm(3)) than acute OVA (7.6 ± 0.2 × 10(3) mm(3)). Dexamethasone treatment before acute OVA abolished the AHR and LAR and significantly reduced eosinophils and the bright-intensity MRI edema from 9.1 ± 1.0 to 6.4 ± 0.3 × 10(3) mm(3).
Conclusion:
We show a temporal relationship between edema and the LAR and their parallel reduction, along with eosinophils and AHR, by dexamethasone. This suggests a close causative association between pulmonary edema and impaired airways function.
Insights
Pulmonary edema is linked to the late asthmatic response (LAR) and airway hyperresponsiveness (AHR). Dexamethasone reduced both edema and AHR, suggesting edema contributes to asthma symptoms.
Area of Science:
- Pulmonary medicine
- Respiratory physiology
- Medical imaging
Background:
- Asthma involves reversible airway obstruction, leukocyte infiltration, airway hyperresponsiveness (AHR), and airway remodeling.
- Pulmonary edema, caused by fluid accumulation, contributes to airway obstruction in asthma.
Purpose of the Study:
- To investigate the temporal relationship between the late asthmatic response (LAR) and pulmonary edema.
- To quantify pulmonary edema using magnetic resonance imaging (MRI) following allergen challenge in a guinea pig model.
Main Methods:
- Ovalbumin (OVA)-sensitized guinea pigs underwent acute or chronic OVA inhalation challenges.
- Airway obstruction was measured using specific airway conductance (sGaw).
- AHR, leukocyte counts, and MRI-based edema signals were assessed post-challenge.
Main Results:
- OVA challenge induced early bronchoconstriction, followed by LAR, AHR, and leukocyte influx.
- MRI detected significant pulmonary edema, peaking at 7 hours post-challenge.
- Dexamethasone treatment reduced AHR, LAR, eosinophils, and pulmonary edema.
Conclusions:
- A temporal association exists between pulmonary edema and the LAR.
- Pulmonary edema and AHR were reduced in parallel by dexamethasone.
- Findings suggest a causative link between pulmonary edema and impaired airway function in asthma.
