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Bleomycin pulmonary fibrosis

Shanon Seger, Manuel Stritt, Enrico Vezzali, Oliver Nayler, Patrick Hess, Peter M A Groenen, Anna K Stalder
Intratracheal administration of bleomycin induces fibrosis in the lung, which is mainly assessed by histopathological grading that is subjective. Current literature highlights the need of reproducible and quantitative pulmonary fibrosis analysis. If some quantitative studies looked at fibrosis parameters separately, none of them quantitatively assessed both aspects: lung tissue remodeling and collagenization. To ensure reliable quantification, support vector machine learning was used on digitalized images to design a fully automated method that analyzes two important aspects of lung fibrosis: (i) areas having substantial tissue remodeling with appearance of dense fibrotic masses and (ii) collagen deposition...
2018: PloS One
Z Tao, J A Huang, S S Chen, Y Hu
Objective: To investigate the treatment effect of carboxyamidotriazole (CAI) on bleomycin induced lung fibrosis in mice, and the potential mechanism involved. Methods: A total of 45 mice were divided into three groups randomly. Blank control group (blank group): after a one-time tail vein injection of saline solution 0.2 ml, mice were given polyethylene glycol 400 (PEG-400) 0.1 ml/10 g by gavage once daily for 14 days; the bleomycin group (BLM group): after a one-time tail vein injection of bleomycin 150 mg/kg, mice were given PEG-400 solution 0...
February 27, 2018: Zhonghua Yi Xue za Zhi [Chinese medical journal]
Yangyang Gu, Bo Huang, Yanfei Yang, Mengdie Qi, Guohua Lu, Dajing Xia, Hequan Li
Idiopathic pulmonary fibrosis (IPF) is a progressive and irreversible lung disease with high mortality rate. The etiology is unknown and treatment choices are limited. Thus, there is great interest to investigate novel agents for IPF therapy. Ibrutinib, BTK, and ITK irreversible inhibitor is a FDA-approved small molecule for the clinical therapy of B cell lymphoma. Its role in pulmonary fibrosis remains unknown. In this study, we investigated the anti-fibrotic activity of ibrutinib. Strikingly, ibrutinib did not inhibit but exacerbated bleomycin-induced pulmonary fibrosis by increased epithelial cell apoptosis, and inflammation in the lung...
March 13, 2018: Inflammation
Dong Weng, Jian-Xia Chen, Hao-Hao Li, Feng Liu, Li-Dan Zhou, Hai-Peng Liu, Rui-Juan Zheng, Yan Jiang, Zhong-Hua Liu, Baoxue Ge
The epithelial-mesenchymal transition (EMT) is a multifunctional cell process involved in the pathogenesis of numerous conditions, including fibrosis and cancer. Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal disease characterized by fibroblast accumulation and collagen deposition in the lungs. The fibroblasts involved in this process partially originate from lung epithelial cells via the EMT. Evidence suggests that the EMT contributes to progression, invasion, and metastasis of various types of cancer...
December 2018: Cell Death Discovery
Ana Valero-Jiménez, Joaquín Zúñiga, José Cisneros, Carina Becerril, Alfonso Salgado, Marco Checa, Ivette Buendía-Roldán, Criselda Mendoza-Milla, Miguel Gaxiola, Annie Pardo, Moisés Selman
Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive lung disease characterized by epithelial cell activation, expansion of the fibroblast population and excessive extracellular matrix accumulation. The mechanisms are incompletely understood but evidence indicates that the deregulation of several proteases contributes to its pathogenesis. Transmembrane protease serine 4 (TMPRSS4) is a novel type II transmembrane serine protease that may promote migration and facilitate epithelial to mesenchymal transition (EMT), two critical processes in the pathogenesis of IPF...
2018: PloS One
Shota Hodono, Akihiro Shimokawa, Neil J Stewart, Yukiko Yamauchi, Renya Nishimori, Mami Yamane, Hirohiko Imai, Hideaki Fujiwara, Atsuomi Kimura
PURPOSE: High Mobility Group Box1 (HMGB1), which is one of the damage-associated molecular pattern molecules relating to various inflammatory diseases, has gained interest as a therapeutic target because of its involvement in wound healing processes. In the present study, we investigated HMGB1 as a potential therapeutic target in a model of lung fibrosis using a preclinical hyperpolarized129 Xe (HPXe) MRI system. METHODS: Lung injury was induced by intra-peritoneal injection of bleomycin (BLM) in 19 mice...
March 9, 2018: Magnetic Resonance in Medical Sciences: MRMS
Won Jai Jung, Sang Yeub Lee, Sue In Choi, Byung-Keun Kim, Eun Joo Lee, Kwang Ho In, Min-Goo Lee
Airway sensory nerves are known to express several receptors and channels that are activated by exogenous and endogenous mediators that cause coughing. Toll-like receptor (TLR) s are expressed in nociceptive neurons and play an important role in neuroinflammation. However, there have been very few studies of TLR expression in lung-derived sensory neurons or their relevance to respiratory symptoms such as cough. We used the bleomycin-induced pulmonary fibrosis model to investigate the change in TLR expression in pulmonary neurons and the association of TLRs with transient receptor potential (TRP) channels in pulmonary neurons...
2018: PloS One
Valérie Besnard, Rania Dagher, Tania Madjer, Audrey Joannes, Madeleine Jaillet, Martin Kolb, Philippe Bonniaud, Lynne A Murray, Matthew A Sleeman, Bruno Crestani
Periplakin is a component of the desmosomes that acts as a cytolinker between intermediate filament scaffolding and the desmosomal plaque. Periplakin is strongly expressed by epithelial cells in the lung and is a target antigen for autoimmunity in idiopathic pulmonary fibrosis. The aim of this study was to determine the role of periplakin during lung injury and remodeling in a mouse model of lung fibrosis induced by bleomycin. We found that periplakin expression was downregulated in the whole lung and in alveolar epithelial cells following bleomycin-induced injury...
March 8, 2018: JCI Insight
Yong-Huai Li, Xiang Wei, Shuang Ji, Shu-Yu Gui, Su-Mei Zhang
The present study aimed to investigate the effects of nucleotide-binding domain leucine-rich repeat protein (NLRP)1/NLRP3 inflammasome pathways on latent viral infection of the respiratory tract. A total of 55 BALB/c mice were assigned to the control, bleomycin (BLM)‑treated, murine cytomegalovirus (MCMV), MCMV+BLM and MCMV+BLM+CD4+ T‑cell groups. The viral loads were detected in the salivary glands, kidney, liver and lung tissues via polymerase chain reaction (PCR). The weight, lung coefficient and hydroxyproline (HYP) were detected...
February 28, 2018: International Journal of Molecular Medicine
Michael McGee, Nicholas Whitehead, Jennifer Martin, Nicholas Collins
INTRODUCTION: While pulmonary arterial hypertension remains an uncommon diagnosis, various therapeutic agents are recognized as important associations. These agents are typically categorized into "definite", "likely", "possible", or "unlikely" to cause pulmonary arterial hypertension, based on the strength of evidence. OBJECTIVE: This review will focus on those therapeutic agents where there is sufficient literature to adequately comment on the role of the agent in the pathogenesis of pulmonary arterial hypertension...
March 6, 2018: Clinical Toxicology
Youhei Takahashi, Atsushi Saito, Hirofumi Chiba, Koji Kuronuma, Kimiyuki Ikeda, Tomofumi Kobayashi, Shigeru Ariki, Motoko Takahashi, Yasushi Sasaki, Hiroki Takahashi
BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is the most frequent and severe form of idiopathic interstitial pneumonias. Although IPF has not been thought to be associated with bacterial communities, recent papers reported the possible role of microbiome composition in IPF. The roles of microbiomes in respiratory functions and as clinical biomarkers for IPF remain unknown. In this study, we aim to identify the relationship between the microbial environment in the lung and clinical findings...
February 27, 2018: Respiratory Research
Ying Meng, Miao-Xia Pan, Bo-Jun Zheng, Yan Chen, Wei Li, Qian-Jie Yang, Ze-Mao Zheng, Na-Na Sun, Yue Zhang, Xu Li
<b><i>Aims:</i></b> The NLRP3 (NOD-like receptor family pyrin domain containing 3) inflammasome, which is activated by reactive oxygen species (ROS) and respressed by autophagy, has been identified as a novel agent of pulmonary fibrosis. Angiotensin II (AngII), the bioactive pro-oxidant in the renin-angiotensin system (RAS), aggravates lung fibrosis. However, the effect of AngII on NLRP3 inflammasome and autophagy in lung fibrosis remains unknown. <i><b>Objective:</b></i> To investigate a potential link between AngII, redox balance, autophagy and the NLRP3 inflammasome, which determines extracellular matrix accumulation in lung fibrosis...
February 27, 2018: Antioxidants & Redox Signaling
Jeongah Song, Woojin Kim, Yong-Bum Kim, Bumseok Kim, Kyuhong Lee
Pulmonary fibrosis is a chronic progressive disease with unknown etiology and has poor prognosis. Polyhexamethyleneguanidine phosphate (PHMG-P) causes acute interstitial pneumonia and pulmonary fibrosis in humans when it exposed to the lung. In a previous study, when rats were exposed to PHMG-P through inhalation for 3 weeks, lung inflammation and fibrosis was observed even after 3 weeks of recovery. In this study, we aimed to determine the time course of PHMG-P-induced lung inflammation and fibrosis. We compared pathological action of PHMG-P with that of bleomycin (BLM) and investigated the mechanism underlying PHMG-P-induced lung inflammation and fibrosis...
February 21, 2018: Toxicology and Applied Pharmacology
Mi-Yeon Jung, Jeong-Han Kang, Danielle M Hernandez, Xueqian Yin, Mahefatiana Andrianifahanana, Youli Wang, Anatilde Gonzalez-Guerrico, Andrew H Limper, Ruth Lupu, Edward B Leof
Evidence is provided that the fibroproliferative actions of TGF-β are dependent on a metabolic adaptation that sustains pathologic growth. Specifically, profibrotic TGF-β signaling is shown to require fatty acid synthase (FASN), an essential anabolic enzyme responsible for the de novo synthesis of fatty acids. With the use of pharmacologic and genetic approaches, we show that TGF-β-stimulated FASN expression is independent of Smad2/3 and is mediated via mammalian target of rapamycin complex 1. In the absence of FASN activity or protein, TGF-β-driven fibrogenic processes are reduced with no apparent toxicity...
February 16, 2018: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
Jos L van der Velden, Darcy E Wagner, Karolyn G Lahue, Sarah T Abdalla, Ying W Lam, Daniel J Weiss, Yvonne M W Janssen-Heininger
Epithelial cells have been suggested as potential drivers of lung fibrosis, although the epithelial-dependent pathways that promote fibrogenesis remain unknown. Extracellular matrix is increasingly recognized as an environment that can drive cellular responses in various pulmonary diseases. In this study, we demonstrate that transforming growth factor- beta (TGF-β1)-stimulated mouse tracheal basal (MTB) cells produce provisional matrix proteins in vitro, which initiate mesenchymal changes in subsequently freshly plated MTB cells via Rho kinase- and c-Jun-N-terminal kinase (JNK1)-dependent processes...
February 22, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
Remo Castro Russo, Benedetta Savino, Massimiliano Mirolo, Chiara Buracchi, Giovanni Germano, Achille Anselmo, Luca Zammataro, Fabio Pasqualini, Alberto Mantovani, Massimo Locati, Mauro M Teixeira
RATIONALE: Chemokines coordinate lung inflammation and fibrosis by acting on chemokine receptors expressed on leukocytes and other cell types. Atypical chemokine receptors (ACKRs) bind, internalize and degrade chemokines, tuning homeostasis and immune responses. ACKR2 recognizes and decreases levels of inflammatory CC chemokines. The role of ACKR2 in fibrogenesis is unknown. OBJECTIVE: Investigate the role of ACKR2 in the context of pulmonary fibrosis. METHODS: The effects of ACKR2 expression and deficiency during inflammation and fibrosis were analyzed using a bleomycin-model of fibrosis, ACKR2-deficient mice, bone marrow chimeras and antibody-mediated leukocyte depletion...
February 22, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
K Griffiths, D M Habiel, J Jaffar, U Binder, W G Darby, C G Hosking, A Skerra, G P Westall, C M Hogaboam, M Foley
Idiopathic pulmonary fibrosis (IPF) is a chronic fibrotic lung disease that is prevalent in individuals >50 years of age, with a median survival of 3-5 years and limited therapeutic options. The disease is characterized by collagen deposition and remodeling of the lung parenchyma in a process that is thought to be driven by collagen-expressing immune and structural cells. The G-protein coupled C-X-C chemokine receptor 4, CXCR4, is a candidate therapeutic target for IPF owing to its role in the recruitment of CXCR4 + fibrocytes from the bone marrow to fibrotic lung tissue and its increased expression levels by structural cells in fibrotic lung tissue...
February 16, 2018: Scientific Reports
Hoda Mojiri-Forushani, Ali Asghar Hemmati, Ali Khodadadi, Mohammad Rashno
OBJECTIVE: Pulmonary fibrosis (PF) is a chronic respiratory system disease. The role of inflammation and angiotensin in the development and progression of PF has previously been demonstrated. Alternation in antifibrotic/profibrotic mediators and NF-κB activation have important roles in PF development. NF-κB, a nuclear factor, induces the transcription of inflammatory and pro-inflammatory cytokines. The aim of this study was to evaluate the effect of valsartan as an angiotensin receptor blocker on IL-4, INF-γ, and NF-κB expression in the treatment of PF...
February 15, 2018: Immunopharmacology and Immunotoxicology
Ji-Min Lee, Masahiro Yoshida, Mi-So Kim, June-Hyuk Lee, Ae-Rin Baek, An Soo Jang, Do Jin Kim, Shunsuke Minagawa, Su Sie Chin, Choon-Sik Park, Jun Araya, Kazuyoshi Kuwano, Sung Woo Park
RATIONALE: Alveolar epithelial cell (AEC) injury leading to cell death is involved in the process of fibrosis development during idiopathic pulmonary fibrosis (IPF). Among regulated/programmed cell death, the excessive apoptosis of AECs has been widely implicated in IPF pathogenesis. Necroptosis is a type of regulated/programmed necrosis. A multiprotein complex composed of receptor-interacting protein kinase-1 and -3 (RIPK1/3) plays a key regulatory role in initiating necroptosis. Although necroptosis participates in disease pathogeneses through the release of damage-associated molecular patterns (DAMPs), its association with IPF progression remains elusive...
February 14, 2018: American Journal of Respiratory Cell and Molecular Biology
Yang Zhou, Chuan Hua He, Daniel S Yang, Tung Nguyen, Yueming Cao, Suchitra Kamle, Chang-Min Lee, Bernadette R Gochuico, William A Gahl, Barry S Shea, Chun Geun Lee, Jack A Elias
Hermansky-Pudlak syndrome (HPS) comprises a group of inherited disorders caused by mutations that alter the function of lysosome-related organelles. Pulmonary fibrosis is the major cause of morbidity and mortality in HPS-1 and HPS-4 patients. However, the mechanisms that underlie the exaggerated injury and fibroproliferative repair responses in HPS have not been adequately defined. In particular, although Galectin-3 (Gal-3) is dysregulated in HPS, its roles in the pathogenesis of HPS have not been adequately defined...
February 2, 2018: Journal of Immunology: Official Journal of the American Association of Immunologists
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