scholarly journals DROSHA-Dependent AIM2 Inflammasome Activation Contributes to Lung Inflammation during Idiopathic Pulmonary Fibrosis

Cells ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 938 ◽  
Author(s):  
Soo Jung Cho ◽  
Kyoung Sook Hong ◽  
Ji Hun Jeong ◽  
Mihye Lee ◽  
Augustine M. K. Choi ◽  
...  
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Protein Expression ◽  
Alveolar Macrophages ◽  
Lung Inflammation ◽  
Mirna Biogenesis ◽  
Inflammasome Activation ◽  
Dependent Lung ◽  
Ribonuclease Iii ◽  
Primary Mouse

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.

scholarly journals DROSHA-Dependent miRNA and AIM2 Inflammasome Activation in Idiopathic Pulmonary Fibrosis

2020 ◽  
Vol 21 (5) ◽  
pp. 1668 ◽  
Author(s):  
Soo Jung Cho ◽  
Mihye Lee ◽  
Heather W. Stout-Delgado ◽  
Jong-Seok Moon
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Lung Inflammation ◽  
Target Gene ◽  
Inflammatory Responses ◽  
Inflammasome Activation ◽  
Ribonuclease Iii ◽  
Double Stranded Dna ◽  
Current Review ◽  
Molecular Patterns

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive interstitial lung disease. Chronic lung inflammation is linked to the pathogenesis of IPF. DROSHA, a class 2 ribonuclease III enzyme, has an important role in the biogenesis of microRNA (miRNA). The function of miRNAs has been identified in the regulation of the target gene or protein related to inflammatory responses via degradation of mRNA or inhibition of translation. The absent-in-melanoma-2 (AIM2) inflammasome is critical for inflammatory responses against cytosolic double stranded DNA (dsDNA) from pathogen-associated molecular patterns (PAMPs) and self-DNA from danger-associated molecular patterns (DAMPs). The AIM2 inflammasome senses double strand DNA (dsDNA) and interacts with the adaptor apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), which recruits pro-caspase-1 and regulates the maturation and secretion of interleukin (IL)-1β and IL-18. A recent study showed that inflammasome activation contributes to lung inflammation and fibrogenesis during IPF. In the current review, we discuss recent advances in our understanding of the DROSHA–miRNA–AIM2 inflammasome axis in the pathogenesis of IPF.

scholarly journals CD71− Alveolar Macrophages in Idiopathic Pulmonary Fibrosis: A Look beyond the Borders of the Disease

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

NHLRC2 mRNA and protein expression in idiopathic pulmonary fibrosis

2021 ◽  
Author(s):  
Mervi Kreus ◽  
Siri Lehtonen ◽  
Johanna Salonen ◽  
Reetta Hinttala ◽  
Riitta Kaarteenaho
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Protein Expression ◽  
Mrna And Protein Expression

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
Keyword(s):  
Multivariate Analysis ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Cigarette Smoking ◽  
Bronchoalveolar Lavage ◽  
Alveolar Macrophages ◽  
Smoking Status ◽  
Physiological Measures ◽  
Multivariate Models ◽  
Normal Volunteers

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.

Low-level laser therapy attenuates lung inflammation and airway remodeling in a murine model of idiopathic pulmonary fibrosis: Relevance to cytokines secretion from lung structural cells

2020 ◽  
Vol 203 ◽  
pp. 111731 ◽  
Author(s):  
Auriléia Aparecida de Brito ◽  
Elaine Cristina da Silveira ◽  
Nicole Cristine Rigonato-Oliveira ◽  
Stephanie Souza Soares ◽  
Maysa Alves Rodrigues Brandao-Rangel ◽  
...  
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Laser Therapy ◽  
Murine Model ◽  
Lung Inflammation ◽  
Airway Remodeling ◽  
Low Level Laser Therapy ◽  
Low Level Laser ◽  
Level Laser ◽  
Cytokines Secretion

NLRP3 Inflammasome Activation Leading to IL-1 – IL-17 Dependent Lung Inflammation and Fibrosis

2014 ◽  
Vol 10 (1) ◽  
pp. 64-70 ◽  
Author(s):  
Dieudonnee Togbe ◽  
Anne-Gaelle Besnard ◽  
Fahima Madouri ◽  
Isabelle Couillin ◽  
Aurelie Gombault ◽  
...  
Keyword(s):  
Nlrp3 Inflammasome ◽  
Lung Inflammation ◽  
Inflammasome Activation ◽  
Dependent Lung ◽  
Nlrp3 Inflammasome Activation

scholarly journals C/EBPβ Acetylation is Involved in Idiopathic Pulmonary Fibrosis

2021 ◽  
Author(s):  
Jingzhu Zhou ◽  
Xiuhai Ji ◽  
yan fen ◽  
Hui ding
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Protein Expression ◽  
Western Blot ◽  
Real Time Pcr ◽  
Lung Fibrosis ◽  
Collagen I ◽  
Fibroblast Foci ◽  
The Relationship ◽  
Control Samples

Abstract Background: IPF is a progressive lung disease, characterized by excessive deposition of ECM. C/EBPβ is involved in the development of pulmonary fibrosis. However, the regulation of C/EBPβ in the context of pulmonary fibrosis is not clear. The study is to identify the C/EBPβ acetylation in IPF．Methods: Lung from six IPF and six control samples were selected in this study. We investigated the expression of C/EBPβ in lungs with Immunochemistry. Moreover, the expression of C/EBPβ mRNA via Real Time-PCR and its protein expression via Western Blot were performed. Meanwhile, the levels of collagen-I and α-SMA as markers of pulmonary fibrosis were also determined by Western Blot. Furthermore, we confirmed the relationship between α-SMA and acetylated C/EBPβ by Co-Immunoprecipitation. Results: We found the elevated C/EBPβ mostly locating in fibroblast foci in lungs of IPF. And the expression of C/EBPβ RNA and protein were obviously increased in IPF (P <0.05), in which the proteins of α-SMA and collagen-I were enhanced (P <0.05). Furthermore, the stronger acetylation of C/EBPβ binging to the α-SMA gene was shown in lung fibrosis (P <0.05). Conclusions: The increased expression of C/EBPβ acetylation associated with α-SMA expression is involved in the development of pulmonary fibrosis.

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