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Murine Model of Allergen Induced Asthma
Published on: May 14, 2012
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Phospholipase A2 in experimental allergic bronchitis: a lesson from mouse and rat models
Rufayda Mruwat1, Saul Yedgar, Iris Lavon
1Department of Biochemistry, Hebrew University Medical School, Jerusalem, Israel.
Plos One
|November 9, 2013
Summary
In asthma models, secretory phospholipase A2 (sPLA2) is crucial for disease development. Inhibiting sPLA2 improved asthma markers, suggesting a key role for sPLA2 in allergic bronchitis.
Area of Science:
- Biochemistry
- Immunology
- Pharmacology
Background:
- Phospholipases A2 (PLA2) initiate inflammatory lipid mediator production.
- In rats, secretory PLA2 (sPLA2) and cytosolic PLA2 (cPLA2) have opposing roles in experimental allergic bronchitis (EAB).
- sPLA2 is elevated in EAB, while cPLA2 is suppressed, with roles reversed upon treatment.
Purpose of the Study:
- To investigate the relevance of mouse and rat models for asthma pathophysiology.
- To compare disease and biochemical markers in mice and rats with ovalbumin-induced EAB.
Main Methods:
- Ovalbumin-induced experimental allergic bronchitis (EAB) was established in mice using established rat protocols.
- Disease and biochemical markers in mice were compared to those observed in rats.
Main Results:
- EAB in mice showed increased lung sPLA2 mRNA (specifically sPLA2gX) and broncho-constricting eicosanoids (CysLTs, PGD2, TBX2).
- Elevated cPLA2 mRNA and PGE2 production were also observed in EAB mice.
- sPLA2 inhibitor treatment ameliorated EAB, reverting both sPLA2 and cPLA2 expression and eicosanoid production.
Conclusions:
- Secretory PLA2 (sPLA2) is pivotal in ovalbumin-induced experimental allergic bronchitis (EAB) in both mice and rats.
- Amelioration of asthma markers in mouse models and human tissues was also seen with cPLA2 inhibition.
- Airway conditions likely require the combined action of multiple essential PLA2s for effective asthma management.
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