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Endotoxin markers in bronchoalveolar lavage fluid of patients with interstitial lung diseases

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 w...

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Detalles Bibliográficos
Autores principales: Szponar, Bogumiła, Larsson, Lennart, Domagała-Kulawik, Joanna
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3551689/
https://www.ncbi.nlm.nih.gov/pubmed/23259971
http://dx.doi.org/10.1186/2049-6958-7-54
Descripción
Sumario: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< 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. 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.