The potential role of antimicrobial peptides from wasp as regulators of the fibrotic process in idiopathic pulmonary fibrosis

Author(s):  
Luísa Coutinho Coelho ◽  
Karina Smidt Simon ◽  
Cesar Augusto Melo-Silva ◽  
Paulo Henrique De Holanda Veloso Junior ◽  
João Paulo Figueiró Longo ◽  
...  
2021 ◽  
Author(s):  
Giovanna Elisiana Carpagnano ◽  
Piera Soccio ◽  
Giulia Scioscia ◽  
Grazia Pia Palladino ◽  
Maria Pia Foschino Barbaro ◽  
...  

2019 ◽  
Vol 20 (22) ◽  
pp. 5618 ◽  
Author(s):  
Paolo Spagnolo ◽  
Philip L. Molyneaux ◽  
Nicol Bernardinello ◽  
Elisabetta Cocconcelli ◽  
Davide Biondini ◽  
...  

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, fibrosing interstitial lung disease that commonly affects older adults and is associated with the histopathological and/or radiological patterns of usual interstitial pneumonia (UIP). Despite significant advances in our understanding of disease pathobiology and natural history, what causes IPF remains unknown. A potential role for infection in the disease’s pathogenesis and progression or as a trigger of acute exacerbation has long been postulated, but initial studies based on traditional culture methods have yielded inconsistent results. The recent application to IPF of culture-independent techniques for microbiological analysis has revealed previously unappreciated alterations of the lung microbiome, as well as an increased bacterial burden in the bronchoalveolar lavage (BAL) of IPF patients, although correlation does not necessarily entail causation. In addition, the lung microbiome remains only partially characterized and further research should investigate organisms other than bacteria and viruses, including fungi. The clarification of the role of the microbiome in the pathogenesis and progression of IPF may potentially allow its manipulation, providing an opportunity for targeted therapeutic intervention.


2008 ◽  
Vol 177 (9) ◽  
pp. 1048-1048 ◽  
Author(s):  
Alfredo N. C. Santana ◽  
Ronaldo A. Kairalla ◽  
Carlos R. R. Carvalho

2017 ◽  
Vol 95 (5) ◽  
pp. 389-393
Author(s):  
V. A. Akhmedov ◽  
O. V. Gaus ◽  
D. V. Petrov

Idiopathic pulmonary fibrosis (IPF) is a most widespread clinic-morphological variant of Idiopathic interstitial pneumonias. Its pathophysiology includes recurrent damages to epithelial cells and anomalous reparative reaction in response to aseptic inflammation in the form of excess fibroblast proliferation. The cause of epithelium damage remains unknown; the involvement of smoking, viral infections, inhaled pollutants, and toxic drug n the initiation of the pathological process is conjectured. Numerous studies of recent years suggest the potential role of gastroesophageal reflux and microaspiration as etiological factors of IPF progression. A brief review of modern views of the relationship between IPF and gastroesophageal reflux is presented.


Pneumologie ◽  
2011 ◽  
Vol 65 (12) ◽  
Author(s):  
S Barkha ◽  
M Gegg ◽  
H Lickert ◽  
M Königshoff

Pneumologie ◽  
2014 ◽  
Vol 68 (06) ◽  
Author(s):  
S Skwarna ◽  
I Henneke ◽  
W Seeger ◽  
T Geiser ◽  
A Günther ◽  
...  

2019 ◽  
Vol 13 (3) ◽  
pp. 166-173 ◽  
Author(s):  
Sergio Harari ◽  
Antonella Caminati ◽  
Marco Confalonieri ◽  
Venerino Poletti ◽  
Carlo Vancheri ◽  
...  

2013 ◽  
Vol 6 (1) ◽  
pp. 20 ◽  
Author(s):  
Deborah L Clarke ◽  
Alan M Carruthers ◽  
Tomas Mustelin ◽  
Lynne A Murray

2011 ◽  
Vol 135 (6) ◽  
pp. 780-788 ◽  
Author(s):  
Robert J. Homer ◽  
Jack A. Elias ◽  
Chun Gun Lee ◽  
Erica Herzog

Abstract Context.—Idiopathic pulmonary fibrosis is a uniformly lethal disease with limited biomarkers and no proven therapeutic intervention short of lung transplantation. Pulmonary fibrosis at one time was thought to be a result of inflammation in the lung. Although some forms of pulmonary fibrosis may result from inflammation, idiopathic pulmonary fibrosis is currently thought to result from cell death primarily and inflammation secondarily. Objective.—To determine the role of inflammation in pulmonary fibrosis in light of our laboratory's published and unpublished research and published literature. Data Sources.—Review based on our laboratory's published and unpublished experimental data with relevant background and clinical context provided. Conclusions.—Although cell death is central to pulmonary fibrosis, the proper cytokine environment leading to macrophage polarization is also critical. Evaluation of this environment is promising both for the development of disease biomarkers and for targets for therapeutic intervention.


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