Eicosanoids and lipocortin-1 in BAL fluid in asthma: effects of smoking and inhaled glucocorticoids

Autor: P. T. W. Van Hal, Henk C. Hoogsteden, Abraham Guz, Shelley E. Overbeek, F.J. Zijlstra, Dirkje S. Postma, Y. Oosterhoff, Kevin Murphy, Susan F Smith
Rok vydání: 1996
Předmět:
Male
bronchial hyperresponsiveness
Physiology
Anti-Inflammatory Agents
DISEASE
MESSENGER-RIBONUCLEIC-ACID
chemistry.chemical_compound
HUMAN-LUNG LAVAGE
Annexin A1
medicine.diagnostic_test
Inhalation
INDUCTION
Respiratory disease
Smoking
Beclomethasone
respiratory system
Middle Aged
LEUKOCYTES
Respiratory Function Tests
medicine.anatomical_structure
Bronchial hyperresponsiveness
Female
Bronchial Hyperreactivity
Bronchoalveolar Lavage Fluid
Histamine
Adult
medicine.medical_specialty
Prostaglandin
6-Ketoprostaglandin F1 alpha
PERIPHERAL-BLOOD
BRONCHOALVEOLAR LAVAGE
MECHANISMS
Physiology (medical)
Internal medicine
Administration
Inhalation
medicine
Humans
Glucocorticoids
RELEASE
Lung
business.industry
medicine.disease
Asthma
respiratory tract diseases
Pulmonary Alveoli
Bronchoalveolar lavage
Endocrinology
Eicosanoid
chemistry
prostaglandin D-2
Immunology
CELLS
Eicosanoids
business
Respiratory tract
Zdroj: Journal of Applied Physiology, 81(2), 548-555. AMER PHYSIOLOGICAL SOC
ISSN: 8750-7587
Popis: Both smoking and asthma are associated with inflammatory changes in the lung, which may be suppressed with the help of exogenous anti-inflammatory drugs or by the endogenous defense system. Lipocortin-1 (LC-1; annexin-1) is an anti-inflammatory protein present in respiratory tract secretions. We report an inverse correlation between extracellular LC-1 concentration and the bronchoconstrictor prostaglandin (PG) D2 [n = 15, Spearman rank correlation coefficient (rS) = -0.597, P < 0.05] in bronchoalveolar lavage fluid (BALF) from allergic asthmatic patients, together with positive correlations between extracellular LC-1 per milliliter BALF and the prostacyclin (PGI2) metabolite 6-keto-PGF1 alpha (n = 15, rS = 0.480, P < 0.05) and between LC-1 per milliliter BALF and concentration of histamine causing a 20% decrease in forced expired volume in 1 s (n = 15, rS = 0.720, P < 0.01) in these subjects. We found no significant difference between the LC-1 concentration in BALF from nonsmoking asthmatic patients who were receiving inhaled glucocorticoid therapy (2 x 100 micrograms beclomethasone 4 times/day for 2.5 yr; median 186 ng LC-1/mg albumin; n = 6) and those who were not (median 126 ng LC-1/mg albumin; n = 12), perhaps because inhaled drugs deposit predominantly in central airways, which are poorly represented in bronchoalveolar lavage. Both asthmatic and healthy volunteers who smoked had higher levels of LC-1 in their BALF than did their nonsmoking counterparts (e.g., asthmatic smokers, median 317 ng LC-1/mg albumin, n = 10; asthmatic nonsmokers, median 162 ng LC-1/mg albumin, n = 18; P < 0.05), perhaps because smokers' lungs contain more alveolar macrophages, cells that release LC-1. We observed a positive correlation between BALF LC-1 and bronchoalveolar lavage cell number (n = 16, rS = 0.821, P < 0.001). Increased extracellular LC-1 may be part of a protective response of the lung to inflammatory insult. Regulation of prostanoid levels might be one mechanism by which LC-1 suppresses inflammation.
Databáze: OpenAIRE
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