Endotoxin markers in bronchoalveolar lavage fluid of patients with interstitial lung diseases
1 Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Rudolfa Weigla 12, 53-114, Wroclaw, Poland
2 Lund University, Department of Laboratory Medicine, Section of Medical Microbiology, Sölvegatan 23, 223 62, Lund, Sweden
3 Warsaw Medical University, Department of Pneumology and Allergology, Banacha 1a, 02-097, Warsaw, Poland
Multidisciplinary Respiratory Medicine 2012, 7:54 doi:10.1186/2049-6958-7-54Published: 22 December 2012
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).
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.
The highest LPS concentration was found in patients with eosinophilic disorders and the lowest in patients with sarcoidosis (p< 0.05) followed by the lung fibrosis and the sr-ILD patients. The difference between LPS in BALf with extremely high eosinophil proportion (> 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.
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.