scholarly journals Screening for Helicobacter pylori in Idiopathic Pulmonary Fibrosis Lung Biopsies

Respiration ◽  
2015 ◽  
Vol 91 (1) ◽  
pp. 3-8 ◽  
Author(s):  
Michael Kreuter ◽  
Detlef Kirsten ◽  
Thomas Bahmer ◽  
Roland Penzel ◽  
Martin Claussen ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Idiopathic Pulmonary Fibrosis Lung ◽  
Lung Biopsies

scholarly journals Peroxiredoxin II Expression and Its Association With Oxidative Stress and Cell Proliferation in Human Idiopathic Pulmonary Fibrosis

2008 ◽  
Vol 56 (10) ◽  
pp. 951-959 ◽  
Author(s):  
Kirsi Vuorinen ◽  
Steffen Ohlmeier ◽  
Outi Leppäranta ◽  
Kaisa Salmenkivi ◽  
Marjukka Myllärniemi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Nitrosative Stress ◽  
Usual Interstitial Pneumonia ◽  
Normal Lung ◽  
Proliferating Cells ◽  
Two Dimensional Gel Electrophoresis ◽  
Western Blots ◽  
Lung Biopsies

Oxidant burden has been suggested to be a contributor to the pathogenesis of idiopathic pulmonary fibrosis (IPF). The study focused on peroxiredoxin (Prx) II, an antioxidant that has been associated with platelet-derived growth factor (PDGF) signaling and consequent cell proliferation. Localization and expression of Prx II, PDGF receptors (PDGFRα, PDGFRβ), Ki67, and nitrotyrosine were assessed in control ( n = 10) and IPF/usual interstitial pneumonia (UIP) ( n = 10) lung biopsies by immunohistochemistry and morphometry. Prx II oxidation was determined by standard and non-reducing Western blots, two-dimensional gel electrophoresis, and mass spectrometry. Prx II localized in the IPF/UIP epithelium and alveolar macrophages. Prx II–positive area in the fibroblastic foci (FF) was smaller than in other parenchymal areas ( p = 0.03) or in the hyperplastic epithelium ( p = 0.01). There was no major Prx II oxidation in IPF/UIP compared with the normal lung. The FF showed only minor immunoreactivity to the PDGFRs; Ki67, a marker of cell proliferation; and nitrotyrosine, a marker of oxidative/nitrosative stress. The results suggest that Prx II oxidation does not relate to the pathogenesis of IPF/UIP and that Prx II, PDGFRs, and proliferating cells colocalize in the IPF/UIP lung. Unexpectedly, FF represented areas of low cell proliferation.

scholarly journals Profibrotic effect of IL-17A and elevated IL-17RA in idiopathic pulmonary fibrosis and rheumatoid arthritis-associated lung disease support a direct role for IL-17A/IL-17RA in human fibrotic interstitial lung disease

2019 ◽  
Vol 316 (3) ◽  
pp. L487-L497 ◽  
Author(s):  
Jie Zhang ◽  
Dan Wang ◽  
Lei Wang ◽  
Shaohua Wang ◽  
Anja C. Roden ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Interstitial Lung Disease ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Lung Disease ◽  
Lung Fibroblasts ◽  
Normal Lung ◽  
T Helper 17 ◽  
Direct Role ◽  
Lung Biopsies

Interleukin (IL)-17 is a T helper 17 cytokine implicated in the pathogenesis of many autoimmune diseases, including rheumatoid arthritis (RA). Although IL-17A has a well-established role in murine pulmonary fibrosis models, its role in the tissue remodeling and fibrosis occurring in idiopathic pulmonary fibrosis (IPF) and RA-associated interstitial lung disease (RA-ILD) is not very well defined. To address this question, we utilized complimentary studies to determine responsiveness of human normal and pathogenic lung fibroblasts to IL-17A and used lung biopsies acquired from patients with IPF and RA-ILD to determine IL-17A receptor (IL-17RA) expression. Both normal and pathogenic IPF lung fibroblasts express functional IL-17RA and respond to IL-17A stimulation with cell proliferation, generation of extracellular matrix (ECM) proteins, and induction of myofibroblast transdifferentiation. Small interfering RNA (siRNA) silencing of IL-17RA attenuated this fibroblast response to IL-17A on ECM production. These fibroblast responses to IL-17A are dependent on NF-κB-mediated signaling. In addition, inhibiting Janus activated kinase (JAK) 2 by either siRNA or a selective pharmacological inhibitor, AZD1480—but not a JAK1/JAK3 selective inhibitor, tofacitinib—also significantly reduced this IL-17A-induced fibrogenic response. Lung biopsies of RA-ILD patients demonstrate significantly higher IL-17RA expression in areas of fibroblast accumulation and fibrosis, compared with either IPF or normal lung tissue. These observations support a direct role for IL-17A in lung fibrosis that may be particularly relevant in the context of RA-ILD.

A novel screening method detects herpesviral DNA in the idiopathic pulmonary fibrosis lung

2011 ◽  
Vol 44 (2) ◽  
pp. 178-186 ◽  
Author(s):  
Ville Pulkkinen ◽  
Kaisa Salmenkivi ◽  
Vuokko L. Kinnula ◽  
Eva Sutinen ◽  
Maija Halme ◽  
...  
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Screening Method ◽  
Idiopathic Pulmonary Fibrosis Lung

scholarly journals Helicobacter pylori seroprevalence in patients with idiopathic pulmonary fibrosis

2013 ◽  
Vol 43 (2) ◽  
pp. 635-638 ◽  
Author(s):  
D. Bennett ◽  
E. Bargagli ◽  
R. M. Refini ◽  
M. S. Campagna ◽  
L. Gennari ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis

scholarly journals Management of patients with idiopathic pulmonary fibrosis in clinical practice: the INSIGHTS-IPF registry

2015 ◽  
Vol 46 (1) ◽  
pp. 186-196 ◽  
Author(s):  
Jürgen Behr ◽  
Michael Kreuter ◽  
Marius M. Hoeper ◽  
Hubert Wirtz ◽  
Jens Klotsche ◽  
...  
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Management Practices ◽  
Severe Disease ◽  
High Resolution Computed Tomography ◽  
Source Data Verification ◽  
New Guidelines ◽  
Lung Biopsies ◽  
Randomised Controlled ◽  
Noninterventional Study

After introduction of the new international guidelines on idiopathic pulmonary fibrosis (IPF) in 2011, we investigated clinical management practices for patients with IPF according to physicians' diagnoses.A prospective, multicenter, noninterventional study with comprehensive quality measures including on-site source data verification was performed in Germany.502 consecutive patients (171 newly diagnosed, 331 prevalent; mean±sd age 68.7±9.4 years, 77.9% males) with a mean disease duration of 2.3±3.5 years were enrolled. IPF diagnosis was based on clinical assessments and high-resolution computed tomography (HRCT) in 90.2%, and on surgical lung biopsy combined with histology in 34.1% (lavage in 61.8%). The median 6-min walk distance was 320 m (mean 268±200 m). The mean forced vital capacity was 72±20% pred and diffusing capacity of the lung for carbon monoxide was 35±15% pred. No drugs were administered in 17.9%, oral steroids in 23.7%, N-acetylcysteine in 33.7%, pirfenidone in 44.2% and other drugs in 4.6% of patients. Only 2.8% of the cohort was listed for lung transplantation.IPF patients were diagnosed in line with the new guidelines. They had more severe disease than those enrolled in recent randomised controlled trials. In addition to HRCT, the frequency of lung biopsies was surprisingly high. Treatment patterns varied substantially.

Regulation of TGF-β storage and activation in the human idiopathic pulmonary fibrosis lung

2012 ◽  
Vol 348 (3) ◽  
pp. 491-503 ◽  
Author(s):  
Outi Leppäranta ◽  
Carla Sens ◽  
Kaisa Salmenkivi ◽  
Vuokko L. Kinnula ◽  
Jorma Keski-Oja ◽  
...  
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Idiopathic Pulmonary Fibrosis Lung
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