Prostaglandin F2α exacerbates ovalbumin-induced chronic pneumonia and attenuates depression in mice

• Published in: Journal of veterinary medical science
• Main Authors: MAEHARA, Toko, FUJIMURA, Atsuki, SEGAWA, Rin, INOUE, Satoshi, SATOH, Hiroshi
• Format: Journal Article
• Language: English
• Published: 05.08.2025
• DOI: 10.1292/jvms.25-0196
• ISSN: 0916-7250; 1347-7439

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.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.