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Panminerva Medica 2019 Sep 24

DOI: 10.23736/S0031-0808.19.03754-6


lingua: Inglese

The effect of cigarette smoking on bronchoalveolar lavage protein profiles from patients with different interstitial lung diseases

Elena BARGAGLI 1 , Paolo CAMELI 1, Alfonso CARLEO 2, Rosa M. REFINI 1, Laura BERGANTINI 1, Miriana D’ALESSANDRO 1, Lucia VIETRI 1, Felice PERILLO 1, Luca VOLTERRANI 3, Paola ROTTOLI 1, Luca BINI 4, Claudia LANDI 4

1 Department of Medical and Surgical Sciences & Neurosciences, Respiratory Diseases and Lung Transplantation Unit, University of Siena, Siena, Italy; 2 Department of Pulmonology , Hannover Medical School, Hannover, Germany; 3 Department of Medical, Surgical and Neuro Sciences, Diagnostic Imaging, University of Siena, Siena, Italy; 4 Laboratory of Functional Proteomics, Department of Life Sciences, University of Siena, Siena, Italy


INTRODUCTION: The proteomic approach applied to the analysis of BAL gives a panorama of the complex network of proteins of different origin and function and their modifications at alveolar level. Cigarette smoking may influence BAL protein composition and it represents the most relevant risk factor for several lung diseases.
EVIDENCE ACQUISITION: This review, for the first time, discussed the literature data about the effects of cigarette smoking on BAL protein composition of healthy subjects and patients affected by interstitial lung diseases (ILD).
EVIDENCE SYNTHESIS: The comparison of BAL protein profiles of smokers and non-smoker healthy controls revealed alterations of proteins related to oxidative stress and protease/antiprotease imbalance (such as alpha 1 antitrypsin, alpha-1-antichymotrypsin, apolipoprotein A1, peroxiredoxin 1 and glutathione S transferase P).
CONCLUSIONS: Smoking exposure leads to a significant dysregulation of a large number of molecular pathways involved in interstitial lung diseases and the proteomic studies applied to the study of BAL of idiopathic pulmonary fibrosis, sarcoidosis and other ILD contributed to clarify the underlying pathogenetic mechanisms facilitating ILD development and biomarker discovery.

KEY WORDS: Bronchoalveolar lavage; Smoke; Intertstital lung diseases; Ethiopathogenesis

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