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Updated: Sep 12, 2025
Murine Model of Allergen Induced Asthma
Published on: May 14, 2012
Prostaglandin F2α exacerbates ovalbumin-induced chronic pneumonia and attenuates depression in mice
Toko Maehara1, Atsuki Fujimura1, Rin Segawa1
1Laboratory of Comparative Veterinary Pharmacology and Toxicology, School of Veterinary Medicine, Iwate University, Iwate Japan.
Abstract:
Prolonged lung inflammation leads to the development of asthma and approximately 27.8% of adult patients with asthma suffer from depression. We examined the effect of the prostaglandin F2α (PGF2α) receptor (FP receptor) agonist, fluprostenol, on ovalbumin (OVA)-induced asthma and asthma-related depression in mice. Repeated fluprostenol+OVA administration increased OVA-induced inflammatory cell infiltration and mRNA expression of inflammatory mediators in the lung. In contrast, in the tail suspension and forced swim tests, fluprostenol+OVA administration significantly reduced the immobile time compared with saline+OVA-administered mice. Fluprostenol+OVA treatment significantly upregulated serotonin 1A receptor and tryptophan hydroxylase in the hippocampus compared with the expression in saline+OVA mice. These results suggest that PGF receptor (FP receptor) stimulation promotes lung inflammation but attenuates depression, possibly via the serotonin pathway.
Insights
Prostaglandin F2α receptor stimulation worsens asthma inflammation but may alleviate depression by affecting serotonin pathways in mice. This research explores the dual role of FP receptor agonists in respiratory and mood disorders.
Area of Science:
- Immunology
- Neuroscience
- Pharmacology
Background:
- Asthma is linked to chronic lung inflammation.
- A significant percentage of adult asthma patients experience depression.
Purpose of the Study:
- To investigate the impact of fluprostenol, a prostaglandin F2α (PGF2α) receptor agonist, on asthma and depression in a mouse model.
- To explore the underlying mechanisms involving serotonin pathways.
Main Methods:
- Ovalbumin (OVA)-induced asthma model in mice.
- Administration of fluprostenol in combination with OVA.
- Assessment of lung inflammation via cell infiltration and inflammatory mediator mRNA expression.
- Behavioral tests (tail suspension, forced swim) to evaluate depression-like behaviors.
- Hippocampal analysis of serotonin 1A receptor and tryptophan hydroxylase expression.
Main Results:
- Repeated fluprostenol+OVA administration exacerbated OVA-induced lung inflammation.
- Fluprostenol+OVA treatment significantly reduced immobility time in behavioral tests, indicating antidepressant effects.
- This treatment upregulated serotonin 1A receptor and tryptophan hydroxylase in the hippocampus.
Conclusions:
- Prostaglandin F2α receptor (FP receptor) stimulation promotes lung inflammation in asthma.
- FP receptor stimulation appears to attenuate depression-like behaviors, potentially through the serotonin pathway.
- These findings suggest a complex, dual role for FP receptor agonists in distinct disease pathologies.
