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Key Role of α-Toxin in Fatal Pneumonia Caused by Staphylococcus aureus Sequence Type 398

2016; American Thoracic Society; Volume: 193; Issue: 2 Linguagem: Inglês

10.1164/rccm.201506-1225le

1535-4970

Mariana Fávero Bonesso, Anthony J. Yeh, Amer E. Villaruz, Hwang‐Soo Joo, Joshua W. McCausland, Carlos Magno Castelo Branco Fortaleza, Ricardo de Souza Cavalcante, Moises T. Sobrinho, Carlos Fernando Ronchi, Gordon Y. C. Cheung, M. L. R. S. Cunha, Michaël Otto,

Neutrophil, Myeloperoxidase and Oxidative Mechanisms

such as hypoventilation and hypereosinophilic syndrome is surprising, and we propose that these findings may indicate novel functions for these gene products relevant to the pathogenesis of lung disease in smokers, a concept that requires further study.Our study has limitations.Subsequent functional investigation is needed to determine how these genes may contribute to the pathogenesis of complex, smoking-related acquired lung disease.This is especially true for genes whereby loss-of-function mutations are implicated in the lung disorder but were up-regulated in healthy smokers in this study.In addition, only a subset of samples were confirmed by RNA sequencing.Bearing these limitations in mind, the data support the concept that genes implicated in rare monogenic lung diseases may have roles in the pathogenesis of smoking-related lung diseases and that smoking-induced changes in expression of these genes could be early molecular events in the development of diverse smoking-related clinical phenotypes.