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Pulmonary arterial muscularization induced by a Th2 immune response
Author(s) -
Grunig Gabriele,
Waal Malefyt Rene,
Emson Claire,
Louten Jennifer,
Voelkel Norbert,
Guignabert Christophe,
Rabinovitch Marlene,
Grunig Ekkehard,
Daley Eleen
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.665.9
Subject(s) - pulmonary hypertension , medicine , hypoxia (environmental) , immune system , lung , pulmonary artery , cardiology , immunology , chemistry , organic chemistry , oxygen
Pulmonary hypertension and pulmonary arterial muscularization (PAmusc) are seen in many parasitic and autoimmune diseases and in chronic inflammatory lung diseases. The goal of this study was to determine the relationships between the immune response, PAmusc, and pulmonary hypertension. Mice were immunized intraperitoneally and exposed to inhaled soluble antigen intermittently for a prolonged period of time or acutely. The prolonged antigen exposure induced dramatic PAmusc that was dependent on the presence of CD4 T cells, IL‐4 and IL‐13. PAmusc was characterized by neo‐intima formation, cell proliferation, and the expression of smooth muscle cell actin. Surprisingly, PAmusc was not associated with increased right ventricular pressures at rest or following challenge with acute hypoxia. The possibility that PAmusc does not necessarily cause pulmonary hypertension has been suggested by clinical observations in children that may quickly regain normal pulmonary arterial pressures after surgical repair of cardiac defects despite the presence of muscularized pulmonary arteries. In conclusion, our data are the first to show experimentally that the adaptive immune response can cause PAmusc and that severe PAmusc and pulmonary hypertension can be dissociated. Supported by: Flight Attendant Medical Research Inst., Stony Wold Herbert Fund, Am. Lung Association of the City of New York