BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a disease of unknown etiology. Biopsy and bronchoalveolar lavage studies have shown, that accumulation of inflammatory cells, particularily neutrophils, in the alveolar space is a relevant feature of the pathogenesis of IPF. This paper adresses the issue of whether the safe and non-invasive method of sputum induction is a suitable tool to study respiratory tract inflammation in IPF. METHODS: In a cross-sectional analysis, 15 IPF patients and 14 healthy, non-smoking subjects underwent sputum induction. Total sputum cell counts, differentials, and the amount of interleukin (IL)-8, granulocyte-macrophage-colony stimulating factor (GM-CSF), and soluble ICAM-1 (sICAM) in sputum supernatant were analyzed. RESULTS: IPF patients had increased sputum neutrophils (60 +/- 6 vs 22 +/- 3%, p = 0.0003), and supernatant concentrations of IL-8 (19 +/- 3 vs. 7 +/- 1 ng/ml, p = 0.0002), GM-CSF (205 +/- 43 vs. 122 +/- 36 pg/ml, p = 0.08) and sICAM (12 +/- 3 vs. 5 +/- 3 ng/ml, p = 0.01), when compared with healthy controls. Sputum IL-8 was correlated with sputum neutrophils (rho = 0.61, p = 0.0006) in all patients. The extent of sputum neutrophilia was also correlated with lung function impairment (vital capacity, % of predicted) in IPF patients (rho = -0.68, p = 0.007). CONCLUSION: These data confirm the established role of neutrophilic inflammation in the pathogenesis of IPF, and show the potential of induced sputum to directly study inflammatory processes and surrogate markers in interstitial lung diseases like IPF.
BACKGROUND:Idiopathic pulmonary fibrosis (IPF) is a disease of unknown etiology. Biopsy and bronchoalveolar lavage studies have shown, that accumulation of inflammatory cells, particularily neutrophils, in the alveolar space is a relevant feature of the pathogenesis of IPF. This paper adresses the issue of whether the safe and non-invasive method of sputum induction is a suitable tool to study respiratory tract inflammation in IPF. METHODS: In a cross-sectional analysis, 15 IPF patients and 14 healthy, non-smoking subjects underwent sputum induction. Total sputum cell counts, differentials, and the amount of interleukin (IL)-8, granulocyte-macrophage-colony stimulating factor (GM-CSF), and soluble ICAM-1 (sICAM) in sputum supernatant were analyzed. RESULTS: IPF patients had increased sputum neutrophils (60 +/- 6 vs 22 +/- 3%, p = 0.0003), and supernatant concentrations of IL-8 (19 +/- 3 vs. 7 +/- 1 ng/ml, p = 0.0002), GM-CSF (205 +/- 43 vs. 122 +/- 36 pg/ml, p = 0.08) and sICAM (12 +/- 3 vs. 5 +/- 3 ng/ml, p = 0.01), when compared with healthy controls. Sputum IL-8 was correlated with sputum neutrophils (rho = 0.61, p = 0.0006) in all patients. The extent of sputum neutrophilia was also correlated with lung function impairment (vital capacity, % of predicted) in IPF patients (rho = -0.68, p = 0.007). CONCLUSION: These data confirm the established role of neutrophilic inflammation in the pathogenesis of IPF, and show the potential of induced sputum to directly study inflammatory processes and surrogate markers in interstitial lung diseases like IPF.
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