Determinants of bronchoalveolar lavage cellularity in idiopathic pulmonary fibrosis

1991 ◽  
Vol 71 (5) ◽  
pp. 1688-1693 ◽  
Author(s):  
D. A. Schwartz ◽  
R. A. Helmers ◽  
C. S. Dayton ◽  
R. K. Merchant ◽  
G. W. Hunninghake

To investigate factors that determine bronchoalveolar lavage (BAL) cellularity in patients with idiopathic pulmonary fibrosis (IPF), we compared BAL cells in patients with IPF (n = 83) to both nonsmoking (n = 111) and smoking (n = 19) normal volunteers. Patients with IPF had higher concentrations of BAL total cells and alveolar macrophages than nonsmoking volunteers and more BAL neutrophils and eosinophils than normal volunteers regardless of smoking status. Among patients with IPF, the numbers of alveolar macrophages, neutrophils, or eosinophils were strongly associated with either smoking status or pack-years of cigarette smoking. In fact, after accounting for cigarette smoking, using multivariate analysis, the only additional factors that were found to be associated with BAL cellularity were age (macrophages and eosinophils) and the percent predicted forced expired volume in 1 s (neutrophils). Additional multivariate models failed to identify a significant relationship between BAL cellularity and either the type of immunosuppressive therapy or other physiological measures of lung function. We conclude that cigarette smoking strongly influences BAL cellularity in patients with IPF. These findings suggest that cigarette smoking may have a role in the pathogenesis of IPF or may adversely affect the prognosis in patients with IPF.

Author(s):  
Eleni Bibaki ◽  
Eirini Vasarmidi ◽  
Chara Koutoulaki ◽  
Semeli Mastrodemou ◽  
Athina Trachalaki ◽  
...  

2013 ◽  
Vol 61 ◽  
pp. 160-163 ◽  
Author(s):  
Foteini Malli ◽  
Fotini Bardaka ◽  
Irene Tsilioni ◽  
Eleni Karetsi ◽  
Konstantinos I. Gourgoulianis ◽  
...  

2021 ◽  
pp. 2101372
Author(s):  
Taro Yasuma ◽  
Corina N. D'Alessandro-Gabazza ◽  
Osamu Hataji ◽  
Tetsu Kobayashi ◽  
Esteban C Gabazza

2017 ◽  
Vol 83 (5) ◽  
Author(s):  
Gaetano Rea ◽  
Giuseppe Fiorentino ◽  
Antonio Corcione ◽  
Maurizia Lanza ◽  
Francesco Perna ◽  
...  

2019 ◽  
Vol 200 (11) ◽  
pp. 1444-1446
Author(s):  
Ermanno Puxeddu ◽  
Daniela Fraboni ◽  
Giuseppe Cillis ◽  
Francesco Cavalli ◽  
Francesco Buccisano ◽  
...  

Cells ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 938 ◽  
Author(s):  
Soo Jung Cho ◽  
Kyoung Sook Hong ◽  
Ji Hun Jeong ◽  
Mihye Lee ◽  
Augustine M. K. Choi ◽  
...  

Idiopathic pulmonary fibrosis (IPF) has been linked to chronic lung inflammation. Drosha ribonuclease III (DROSHA), a class 2 ribonuclease III enzyme, plays a key role in microRNA (miRNA) biogenesis. However, the mechanisms by which DROSHA affects the lung inflammation during idiopathic pulmonary fibrosis (IPF) remain unclear. Here, we demonstrate that DROSHA regulates the absent in melanoma 2 (AIM2) inflammasome activation during idiopathic pulmonary fibrosis (IPF). Both DROSHA and AIM2 protein expression were elevated in alveolar macrophages of patients with IPF. We also found that DROSHA and AIM2 protein expression were increased in alveolar macrophages of lung tissues in a mouse model of bleomycin-induced pulmonary fibrosis. DROSHA deficiency suppressed AIM2 inflammasome-dependent caspase-1 activation and interleukin (IL)-1β and IL-18 secretion in primary mouse alveolar macrophages and bone marrow-derived macrophages (BMDMs). Transduction of microRNA (miRNA) increased the formation of the adaptor apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) specks, which is required for AIM2 inflammasome activation in BMDMs. Our results suggest that DROSHA promotes AIM2 inflammasome activation-dependent lung inflammation during IPF.


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