title: Asthma causes inflammation of human pulmonary arteries and decreases vasodilatation induced by prostaglandin I2analogs.
abstract: OBJECTIVE
  Asthma is a chronic inflammatory disease associated with increased cardiovascular events. This study assesses the presence of inflammation and the vascular reactivity of pulmonary arteries in patients with acute asthma.
  
  
  METHODS
  Rings of human pulmonary arteries obtained from non-asthmatic and asthmatic patients were set up in organ bath for vascular tone monitoring. Reactivity was induced by vasoconstrictor and vasodilator agents. Protein expression of inflammatory markers was detected by western blot. Prostanoid releases and cyclic adenosine monophosphate (cAMP) levels were quantified using specific enzymatic kits.
  
  
  RESULTS
  Protein expression of cluster of differentiation 68, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and cyclooxygenase-2 was significantly increased in arteries obtained from asthmatic patients. These effects were accompanied by an alteration of vasodilatation induced by iloprost and treprostinil, a decrease in cAMP levels and an increase in prostaglandin (PG) E2and PGI2synthesis. The use of forskolin (50 µmol/L) has restored the vasodilatation and cAMP release. No difference was observed between the two groups in reactivity induced by norepinephrine, angiotensin II, PGE2, KCl, sodium nitroprusside, and acetylcholine.
  
  
  CONCLUSIONS
  Acute asthma causes inflammation of pulmonary arteries and decreases vasodilation induced by PGI2analogs through the impairment of cAMP pathway.
authors.affiliation: a Laboratory of Cardiovascular Genetic and Nutritional Diseases , University Setif 1 , Algeria.|b Faculty of Medicine, University Setif 1 , Algeria.
authors.forename: Nabil
authors.identifier: http://orcid.org/0000-0002-1616-2210
authors.initials: N
authors.lastname: Foudi
authors.affiliation: b Faculty of Medicine, University Setif 1 , Algeria.
authors.forename: Aouatef
authors.initials: A
authors.lastname: Badi
authors.affiliation: a Laboratory of Cardiovascular Genetic and Nutritional Diseases , University Setif 1 , Algeria.|b Faculty of Medicine, University Setif 1 , Algeria.
authors.forename: Mounira
authors.initials: M
authors.lastname: Amrane
authors.affiliation: c Laboratory of Functional Genomics in Atherothrombosis , Lyon , France.
authors.forename: Wassim
authors.initials: W
authors.lastname: Hodroj
mesh_terms: D000328:Adult; D001249:Asthma / Q000276:immunology / Q000503:physiopathology*; D015415:Biomarkers; D005576:Colforsin / Q000494:pharmacology; D000242:Cyclic AMP / Q000037:antagonists & inhibitors; D051546:Cyclooxygenase 2 / Q000096:biosynthesis; D015232:Dinoprostone / Q000096:biosynthesis; D011464:Epoprostenol / Q000031:analogs & derivatives / Q000494:pharmacology; D005260:Female; D006801:Humans; D016285:Iloprost / Q000494:pharmacology; D007249:Inflammation / Q000276:immunology; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis; D008297:Male; D008875:Middle Aged; D011453:Prostaglandins / Q000276:immunology; D044062:Prostaglandins I / Q000494:pharmacology*; D011465:Prostaglandins, Synthetic / Q000494:pharmacology*; D011651:Pulmonary Artery / Q000187:drug effects*; D019010:Vascular Cell Adhesion Molecule-1 / Q000096:biosynthesis; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects*
chemical_list: D015415:Biomarkers; D011453:Prostaglandins; D044062:Prostaglandins I; D011465:Prostaglandins, Synthetic; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D005576:Colforsin; D011464:Epoprostenol; D000242:Cyclic AMP; D051546:Cyclooxygenase 2; D016285:Iloprost; D015232:Dinoprostone; C427248:treprostinil
keywords: Asthma; prostaglandins; pulmonary arteries; vasoconstriction; vasodilatation