Prostaglandin D₂ and T(H)2 inflammation in the pathogenesis of bronchial asthma

[nanonug]

1. Korean J Intern Med. 2011 Mar;26(1):8-18. Epub 2011 Mar 2.

Prostaglandin D₂ and T(H)2 inflammation in the pathogenesis of bronchial asthma.

Arima M, Fukuda T.

Department of Developmental Genetics (H2), Chiba University Graduate School of
Medicine, Chiba, Japan. masaarima@faculty.chiba-u.jp

Erratum in
Korean J Intern Med. 2011 Jun;26(2):253.

Prostaglandin D₂ (PGD₂) is a major prostanoid, produced mainly by mast cells, in
allergic diseases, including bronchial asthma. PGD₂-induced vasodilatation and
increased permeability are well-known classical effects that may be involved in
allergic inflammation. Recently, novel functions of PGD₂ have been identified. To
date, D prostanoid receptor (DP) and chemoattractant receptor homologous molecule
expressed on T(H)2 cells (CRTH2) have been shown to be major PGD₂-related
receptors. These two receptors have pivotal roles mediating allergic diseases by
regulating the functions of various cell types, such as T(H)2 cells, eosinophils,
basophils, mast cells, dendritic cells, and epithelial cells. This review will
focus on the current understanding of the roles of PGD₂ and its metabolites in
T(H)2 inflammation and the pathogenesis of bronchial asthma.

PMCID: PMC3056260
PMID: 21437156 [PubMed - indexed for MEDLINE]

 

[alex3619]

Manipulation of prostaglandin synthesis was one of the things I was involved in, as patient and guinea pig, in the early 1990s. It can reduce symptoms, it does not cure the disorder though. Look at the works of Andriya Martinovic, who has one paper on this on Pubmed, though the topic is eicosanoid modulation - prostaglandins are one type of eicosanoid.

Prostaglandins are cellular hormones - autocrine and paracrine hormones, though not endocrine or exocrine.

Bye, Alex

 

[nanonug]

Manipulation of prostaglandin synthesis was one of the things I was involved in, as patient and guinea pig, in the early 1990s. It can reduce symptoms, it does not cure the disorder though.

This is very interesting. I put this abstract in here because there is thing that appears common in ME/CFS, which is Th2 dominance. On the other hand, PGD2 is one of the substances released by mast cells, but not the only one. If ME/CFS is indeed a mast cell disorder, it might explain why eicosanoid modulation helps but doesn't fully solve the problem.