Open AccessEndotoxin markers in bronchoalveolar lavage fluid of patients with interstitial lung diseases
Author(s) -
Bogumiła Szponar,
Lennart Larsson,
Joanna DomagałaKulawik
Publication year - 2012
Publication title -
multidisciplinary respiratory medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.72
H-Index - 28
eISSN - 2049-6958
pISSN - 1828-695X
DOI - 10.4081/mrm.2012.641
Subject(s) - bronchoalveolar lavage , medicine , eosinophil , sarcoidosis , immunology , pulmonary fibrosis , lung , idiopathic pulmonary fibrosis , eosinophilic , diffuse panbronchiolitis , pathology , interstitial lung disease , gastroenterology , asthma , biology , antibiotics , erythromycin , microbiology and biotechnology
Background: Exposure to inhaled endotoxins (lipopolysaccharides, LPS) of Gram-negative bacteria commonly found in indoor environments and assessed in secondary tobacco smoke, has been associated with airway inflammation and asthma exacerbation. The bronchoalveolar lavage fluid (BALf) from patients with interstitial lung diseases (sarcoidosis, lung fibrosis, smoking-related ILD, eosinophilic disorders) was analyzed for the markers of lipopolysaccharide (LPS, endotoxin). Methods: BALf was obtained from patients with diffuse lung diseases: idiopathic pulmonary fibrosis (n = 42), sarcoidosis (n = 22), smoking-related-ILD (n = 11) and eosinophilic disorders (n = 8). Total cell count and differential cell count were performed. In addition, samples were analyzed for 3-hydroxy fatty acids (3-OHFAs) of 10–18 carbon chain lengths, as markers of LPS, by gas chromatography-tandem mass spectrometry. Results: The highest LPS concentration was found in patients with eosinophilic disorders and the lowest in patients with sarcoidosis (p 25%) and those with lower proportion was also significant (p = 0.014). A significant correlation was found between LPS and eosinophils, but not between LPS and lymphocytes, neutrophils, or macrophages count. Conclusions: A positive relationship of LPS and eosinophilic pulmonary disorders may be linked to a persistent eosinophil activation mediated by Th2 pathway: chronic endotoxin exposure would intensify Th2 pathway resulting in fibrosis and, at the same time, eosinophil stimulation, and hence in eosinophilic pulmonary disorders.