When the nasal mucosa of allergic rhinitis patients is exposed to antigens, lipid metabolites such as prostaglandins and leukotrienes are released from immune cells. These cause an increase in blood flow in the nasal mucosa and collapse of the blood vessel wall barrier, thickening the nasal mucosa and causing nasal congestion. A variety of lipid metabolites are produced in patients' nasal secretions, but the effect of many of them on nasal congestion was unknown.

　In past research, the research group detected a lipid called 15-hydroxyeicosatrienoic acid (15-HETrE), a metabolite of dihomo-gamma-linolenic acid, in the nasal secretions of allergic rhinitis model mice. This time, we evaluated the effect of 5-HETrE on nasal congestion.

　In experiments, 15-HETrE caused mice to have symptoms related to breathing difficulties, such as lying down and abdominal breathing, as well as narrowing of the nasal passages, leading to nasal congestion. The mechanism behind this was found to be that 15-HETrE relaxes nasal mucosal blood vessels and increases permeability. Furthermore, 15-HETrE was found to relax blood vessels in mice via prostaglandin D2 receptor (DP) and prostaglandin I2 receptor (IP).

　Prostaglandin D2 is a lipid metabolite that is the target of drug discovery as a factor that worsens nasal congestion. This discovery suggests that a metabolite of dihomo-gamma-linolenic acid, which has not received much attention so far, is involved in the classical lipid acceptance pathway and worsens nasal congestion. It is hoped that this will lead to the development of new treatments.

Paper information:【Allergology International】15-Hydroxyeicosatrienoic acid induces nasal congestion by changing vascular functions in mice