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Diesel Exhaust Particle (DEP)‐Induced Acute Loss of Respiratory Neutral Endopeptidase
Author(s) -
Wong Simon S.,
Sun Ni,
Miller Hugh B,
Desmarais Thomas J,
Witten Mark L,
Burgess Jefferey L
Publication year - 2009
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.23.1_supplement.778.7
Subject(s) - exhaled breath condensate , vital capacity , spirometry , respiratory system , sputum , diesel exhaust , lung volumes , neprilysin , medicine , pulmonary function testing , chemistry , lung , immunology , lung function , diesel fuel , pathology , asthma , diffusing capacity , biochemistry , enzyme , tuberculosis , organic chemistry
Neutral endopeptidase (NEP) is a key cell surface peptidase in the maintenance of airway homeostasis involving the development of pulmonary disorders. However, little information is available about the effect of respiratory particles on airway NEP. Cross‐shift spirometry and sputum NEP were measured on twelve normal subjects following acute diesel exhaust exposure. A significant increase in soluble NEP in sputum was observed with 31% average net increases when compared with pre‐exposure. Pearson's correlation analyses indicated that changes in sputum NEP activity were significantly associated with diesel exhaust particle (DEP) exposure. DEP exposure also induced a significant decline in forced expiratory volume in one second (FEV1, 4.03 ± 0.29 vs. 3.78 ± 0.29; p = 0.005 pre‐ vs. post exposure) and forced vital capacity (FVC, 5.16 ± 0.36 vs. 4.86 ± 0.39, p = 0.017), which were significantly associated with sputum NEP activity, not with DEP exposure. The changes in NEP activity may be an accurate endpoint for DEP exposure, be mechanistically linked to lung function, and indicate a greater susceptibility to the risk of pulmonary diseases.