Plasma Concentrations of Prostaglandins E₂ and F_2α in Asthmatic Patients

Abstract

Plasma concentrations of prostaglandins E₂ (PGE₂) and F_2α (PGF_2α) are studied in venous and arterial blood in 14 healthy subjects and 32 asthmatic patients. In the asthmatic patients we found: (1) a good correlation between PGE₂ concentration in venous blood and the seriousness of the airway obstruction; (2) a good correlation between PGE₂ and PGF_2α in the arterial blood, but not in the venous blood; (3) a decrease in the arterial concentrations of PGE₂ and PGF_2α after fenoterol-induced bronchodilatation, but the variations of PGE₂ and PGF_2α still correlate. None of these results were obtained in normal subjects. It seems that the asthmatic allergic patient has a disorder of the metabolism of prostaglandins in the lungs; however, the results obtained do not allow us to say if it is a causal condition or a metabolic consequence of the bronchospasm. Concerning the venous blood, there could be an increase in the peripheral production of PGE₂ which might result from the hypoxemia following airway obstruction.

Augmentation of allergic inflammation in prostanoid IP receptor deficient mice

“…Therefore, we can conclude that PGD 2 plays a role as a causative substance in allergic inflammation of airway. In addition to PGD 2 , other prostanoids, such as PGF 2α and thromboxane A 2 , may play pathophysiological roles in allergic bronchoconstriction (Godard et al ., 1981; Lahti et al ., 1983; Montuschi et al ., 1999; Schulman et al ., 1981; Yamasaki et al ., 1997). In contrast, PGE 2 and PGI 2 were reported to be suppressive mediators in allergic reactions.…”

“…These data suggest the dominance of Th2 response in IP receptor deficient mice over the Th1 response. Since there are many findings to indicate the importance of the Th1 and Th2 balance in allergic reactions (Calder, 2000; Godard et al ., 1981; Prahalad, 2000; Ray & Cohn, 2000), further experiments are necessary to clarify the role of PGI 2 especially concerning the balance between Th1 and Th2 cells during immunological processes. In addition, the activities of other immunological cells including antigen presenting cells, B cells and others were not studied.…”

Prostaglandin as a Target Molecule for Pharmacotherapy of Allergic Inflammatory Diseases

“…Most researchers agree with the production of several types of PGs during allergic reaction in human and experimental animals. [16][17][18][19][20] But each researcher has failed to obtain consensus in terms of the effect of the PG inhibitors on allergic response and the magnitude of allergic response caused by each PG. So, in this review, we focused on the experimental results employing PG synthesis inhibitor, indomethacin, and PG receptor gene manipulated mice on allergic reaction in mice.…”