scholarly journals Effect of Total Flavonoids of Oxytropis falcata Bunge on the Expression of p-JAK1-and p-STAT1-Related Proteins in Idiopathic Pulmonary Fibrosis

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Yan-jun Wang ◽  
Yang Li ◽  
Xue-lin Wang ◽  
Xin-ze Li ◽  
Yan-wen Chen ◽  
...  
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Lung Tissue ◽  
Positive Control ◽  
Prednisolone Acetate ◽  
High Dose ◽  
Total Flavonoids ◽  
Transmission Electron ◽  
Kg Medium ◽  
Related Proteins

Objective. The study aimed to explore the effect of total flavonoids of Oxytropis falcata Bunge (FOFB) on the expression of p-JAK1/p-STAT1 and SOCS3 proteins in idiopathic pulmonary fibrosis (IPF). Methods. Rats model with IPF was established by one-off intratracheal injection of bleomycin (BLM, 5 mg/kg). After 14 days, the same volume of low dose (100 mg/kg), medium dose (200 mg/kg), and high dose (400 mg/kg) of FOFB and prednisolone acetate (20 mg/kg) as positive control drugs, as well as normal saline, were orally administered to rats once a day for 28 consecutive days. Subsequently, the degree of fibrosis and alveolitis in rat lung tissue was observed, respectively, by HE and Masson staining. Further more, observing the ultrastructure of lung tissue by transmission electron microscopy (TEM), the detection of JAK/STAT pathway related indicators including p-JAK1, p-STAT1, and SOCS3 with immunohistochemistry and SOCS3 with real-time PCR (RT-PCR) was performed. Results. Compared with the BLM group, the degree of alveolitis and fibrosis improved significantly, and the expression of p-JAK1 and p-STAT1 decreased; conversely, the expression of SOCS3 increased in the treatment group. Conclusion. IPF causes high expression of p-JAK1 and p-STAT1 and low expression of SOCS3. FOFB can play a role in the treatment of IPF via upregulating SOCS3 and downregulating p-JAK1 and p-STAT1.

Macrophage migration inhibitory factor in lung tissue of idiopathic pulmonary fibrosis patients

2016 ◽  
Vol 42 (5) ◽  
pp. 263-266 ◽  
Author(s):  
Carmela Olivieri ◽  
Elena Bargagli ◽  
Simona Inghilleri ◽  
Ilaria Campo ◽  
Marcella Cintorino ◽  
...  
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Lung Tissue ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Macrophage Migration

Pathology of Asbestosis—An Update of the Diagnostic Criteria: Report of the Asbestosis Committee of the College of American Pathologists and Pulmonary Pathology Society

2010 ◽  
Vol 134 (3) ◽  
pp. 462-480 ◽  
Author(s):  
Victor L. Roggli ◽  
Allen R. Gibbs ◽  
Richard Attanoos ◽  
Andrew Churg ◽  
Helmut Popper ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Differential Diagnosis ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Interstitial Fibrosis ◽  
Fiber Analysis ◽  
Transmission Electron ◽  
Respiratory Bronchiole ◽  
Slow Tempo

Abstract Asbestosis is defined as diffuse pulmonary fibrosis caused by the inhalation of excessive amounts of asbestos fibers. Pathologically, both pulmonary fibrosis of a particular pattern and evidence of excess asbestos in the lungs must be present. Clinically, the disease usually progresses slowly, with a typical latent period of more than 20 years from first exposure to onset of symptoms. Differential Diagnosis: Idiopathic Pulmonary Fibrosis The pulmonary fibrosis of asbestosis is interstitial and has a basal subpleural distribution, similar to that seen in idiopathic pulmonary fibrosis, which is the principal differential diagnosis. However, there are differences between the 2 diseases apart from the presence or absence of asbestos. First, the interstitial fibrosis of asbestosis is accompanied by very little inflammation, which, although not marked, is better developed in idiopathic pulmonary fibrosis. Second, in keeping with the slow tempo of the disease, the fibroblastic foci that characterize idiopathic pulmonary fibrosis are infrequent in asbestosis. Third, asbestosis is almost always accompanied by mild fibrosis of the visceral pleura, a feature that is rare in idiopathic pulmonary fibrosis. Differential Diagnosis: Respiratory Bronchiolitis Asbestosis is believed to start in the region of the respiratory bronchiole and gradually extends outward to involve more and more of the lung acinus, until the separate foci of fibrosis link, resulting in the characteristically diffuse pattern of the disease. These early stages of the disease are diagnostically problematic because similar centriacinar fibrosis is often seen in cigarette smokers and is characteristic of mixed-dust pneumoconiosis. Fibrosis limited to the walls of the bronchioles does not represent asbestosis. Role of Asbestos Bodies Histologic evidence of asbestos inhalation is provided by the identification of asbestos bodies either lying freely in the air spaces or embedded in the interstitial fibrosis. Asbestos bodies are distinguished from other ferruginous bodies by their thin, transparent core. Two or more asbestos bodies per square centimeter of a 5-μm-thick lung section, in combination with interstitial fibrosis of the appropriate pattern, are indicative of asbestosis. Fewer asbestos bodies do not necessarily exclude a diagnosis of asbestosis, but evidence of excess asbestos would then require quantitative studies performed on lung digests. Role of Fiber Analysis Quantification of asbestos load may be performed on lung digests or bronchoalveolar lavage material, employing either light microscopy, scanning electron microscopy, or transmission electron microscopy. Whichever technique is employed, the results are only dependable if the laboratory is well practiced in the method chosen, frequently performs such analyses, and the results are compared with those obtained by the same laboratory applying the same technique to a control population.

scholarly journals Effect of dermatan sulphate on a C57-mouse model of pulmonary fibrosis

2019 ◽  
Vol 47 (6) ◽  
pp. 2655-2665
Author(s):  
Jianfeng Xu ◽  
Wei Li ◽  
Shufen Xu ◽  
Weiyang Gao ◽  
Zhenyu Yu
Keyword(s):  
Pulmonary Fibrosis ◽  
Mouse Model ◽  
Lung Tissue ◽  
Interstitial Fibrosis ◽  
Group Versus ◽  
Tissue Type ◽  
Control Group ◽  
Prednisolone Acetate ◽  
Sulphate Group ◽  
Dermatan Sulphate

Objective To test the antifibrotic effect of dermatan sulphate in a bleomycin-induced mouse model of pulmonary fibrosis. Methods C57 mice were randomly divided into four experimental groups: saline-treated control group, bleomycin-induced fibrosis group, prednisolone acetate group and dermatan sulphate group. Lungs were assessed using the lung index, and the extent of interstitial fibrosis was graded using histopathological observation of haematoxylin & eosin-stained lung tissue. Lung tissue hydroxyproline levels and blood fibrinogen levels were measured using a hydroxyproline colorimetric kit and the Clauss fibrinogen assay, respectively. Tissue-type plasminogen activator (tPA) was measured using a chromogenic tPA assay kit. Results Lung index values were significantly lower in the dermatan sulphate group versus the fibrosis group. Histopathological analyses revealed that dermatan sulphate treatment ameliorated the increased inflammatory cell infiltration, and attenuated the reduction in interstitial thickening, associated with bleomycin-induced fibrosis. Hydroxyproline and fibrinogen levels were decreased in the dermatan sulphate group versus the fibrosis model group. Dermatan sulphate treatment was associated with increased tPA levels versus controls and the fibrosis group. Conclusions Damage associated with bleomycin-induced pulmonary fibrosis was alleviated by dermatan sulphate.

Essential trace element levels in lung tissue of idiopathic pulmonary fibrosis patients: A case control study

2020 ◽  
Vol 37 (10) ◽  
pp. 188-193
Author(s):  
Cebrail ÅžimÅŸek ◽  
Gülden Sarı ◽  
Bilge Akgündüz ◽  
Yetkin AÄŸaçkıran ◽  
V. Ali Türksoy ◽  
...  
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Trace Element ◽  
Lung Tissue ◽  
Case Control Study ◽  
Case Control ◽  
Essential Trace Element ◽  
Trace Element Levels ◽  
Control Study

scholarly journals CD8+ T lymphocytes in lung tissue from patients with idiopathic pulmonary fibrosis

2005 ◽  
Vol 6 (1) ◽  
Author(s):  
Zoe Daniil ◽  
Panagiota Kitsanta ◽  
George Kapotsis ◽  
Maria Mathioudaki ◽  
Androniki Kollintza ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Lung Tissue ◽  
Cd8 T Lymphocytes

scholarly journals CD247, a Potential T Cell–Derived Disease Severity and Prognostic Biomarker in Patients With Idiopathic Pulmonary Fibrosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Yupeng Li ◽  
Shibin Chen ◽  
Xincheng Li ◽  
Xue Wang ◽  
Huiwen Li ◽  
...  
Keyword(s):  
T Cell ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Disease Severity ◽  
Lung Tissue ◽  
Prognostic Biomarker ◽  
Pearson Correlation ◽  
Tissue Samples ◽  
Cell Surface Glycoprotein ◽  
Low Expression

BackgroundIdiopathic pulmonary fibrosis (IPF) has high mortality worldwide. The CD247 molecule (CD247, as known as T-cell surface glycoprotein CD3 zeta chain) has been reported as a susceptibility locus in systemic sclerosis, but its correlation with IPF remains unclear.MethodsDatasets were acquired by researching the Gene Expression Omnibus (GEO). CD247 was identified as the hub gene associated with percent predicted diffusion capacity of the lung for carbon monoxide (Dlco% predicted) and prognosis according to Pearson correlation, logistic regression, and survival analysis.ResultsCD247 is significantly downregulated in patients with IPF compared with controls in both blood and lung tissue samples. Moreover, CD247 is significantly positively associated with Dlco% predicted in blood and lung tissue samples. Patients with low-expression CD247 had shorter transplant-free survival (TFS) time and more composite end-point events (CEP, death, or decline in FVC >10% over a 6-month period) compared with patients with high-expression CD247 (blood). Moreover, in the follow-up 1st, 3rd, 6th, and 12th months, low expression of CD247 was still the risk factor of CEP in the GSE93606 dataset (blood). Thirteen genes were found to interact with CD247 according to the protein–protein interaction network, and the 14 genes including CD247 were associated with the functions of T cells and natural killer (NK) cells such as PD-L1 expression and PD-1 checkpoint pathway and NK cell-mediated cytotoxicity. Furthermore, we also found that a low expression of CD247 might be associated with a lower activity of TIL (tumor-infiltrating lymphocytes), checkpoint, and cytolytic activity and a higher activity of macrophages and neutrophils.ConclusionThese results imply that CD247 may be a potential T cell-derived disease severity and prognostic biomarker for IPF.

scholarly journals Efficacy of low dose pirfenidone in idiopathic pulmonary fibrosis: real world experience from a tertiary university hospital

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Myung Jin Song ◽  
Sung Woo Moon ◽  
Ji Soo Choi ◽  
Sang Hoon Lee ◽  
Su Hwan Lee ◽  
...  
Keyword(s):  
Gastrointestinal Tract ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Adverse Events ◽  
Dose Reduction ◽  
Dose Group ◽  
Low Dose ◽  
High Dose Group ◽  
High Dose ◽  
Significant Difference

AbstractPirfenidone is an antifibrotic agent that has been proven to slow down the progression of idiopathic pulmonary fibrosis (IPF). The aim of this study was to evaluate the efficacy of low-dose pirfenidone (that is, less than 1200 mg/day). We retrospectively reviewed the medical records of patients with IPF. The patients were divided into the following three groups, those who were not treated with pirfenidone (control) and those who were treated with pirfenidone at doses < 1200 mg/day (low-dose group) and ≥ 1200 mg/day (high-dose group). The adjusted mean changes in forced vital capacity (FVC) in 1 year were − 200.7, − 88.4, and − 94.7 mL in the control, low-dose, and high-dose groups (p = 0.021). The FVC declined more significantly in the control group than in the low-dose and high-dose groups. No significant difference in FVC change was observed between the low-dose and high-dose groups. Dyspepsia, anorexia, and nausea were significantly more frequent in the low-dose than in the high-dose group, suggesting that dose reduction is attributed to gastrointestinal tract-related adverse events. Dose reduction may help patients to better control gastrointestinal tract-related adverse events; continuing taking the medication at low doses is also expected to be effective in reducing the FVC decline.

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