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Alveolar epithelial injury

Shujun Zhou, Gui Wang, Wenbin Zhang
The present study aimed to investigate the effects of the Toll-like receptor (TLR)4/myeloid differentiation primary response (MyD)88 signaling pathway on sepsis-associated acute respiratory distress syndrome (ARDS) in rats, and the involvement of macrophage activation and the inflammatory response. A total of 36 specific pathogen-free male Sprague-Dawley rats were selected to establish the rat model of sepsis-associated ARDS using cecal ligation and puncture (CLP). Rats were assigned into the Ab (anti-TLR4 monoclonal antibody)-CLP, CLP and Sham groups...
April 2018: Experimental and Therapeutic Medicine
Hari R Desu, Laura A Thoma, George C Wood
PURPOSE: Acute lung injury (ALI) is a fatal syndrome in critically ill patients. It is characterized by lung edema and inflammation. Numerous pro-inflammatory mediators are released into alveoli. Among them, interleukin-1beta (IL-1β) causes an increase in solute permeability across the alveolar-capillary barrier leading to edema. It activates key effector cells (alveolar epithelial and endothelial cells) releasing inflammatory chemokines and cytokines. The purpose of the study was to demonstrate that nebulized liposomes inhibit ALI in vivo...
March 13, 2018: Pharmaceutical Research
Nicole L Jansing, Neesirg Patel, Jazalle McClendon, Elizabeth F Redente, Peter M Henson, Rubin M Tuder, Dallas M Hyde, Jens R Nyengaard, Rachel L Zemans
No abstract text is available yet for this article.
March 13, 2018: American Journal of Respiratory and Critical Care Medicine
Hui-Lun Lu, Xin-Yan Huang, Yi-Feng Luo, Wei-Ping Tan, Pei-Fen Chen, Yu-Biao Guo
The goal of this study was to investigate the role of M1 macrophages in acute lung injury (ALI). To address this, we used LPS-treated wildtype and CD11b-DTR mice, and examined their M1 macrophage levels, and the extent of their inflammation and pulmonary injuries. In addition, we evaluated pulmonary function by measuring the expressions of SP-A and SP-B in infiltrated M1 macrophages. Finally, we co-cultured the mouse type II-like alveolar epithelial cells (AT-II) and mouse pulmonary microvascular endothelial cells (PMECs) with M1 macrophages in the presence of TNF-α or H2 O2 and assessed them for viability and apoptosis...
March 12, 2018: Bioscience Reports
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
Bingji Jin, Hong Jin
The epithelial sodium channel (ENaC) and mitogen-activated protein kinase (MAPK) pathway have been reported to be associated with the progression of acute lung injury (ALI). Oxymatrine (OMT) alone or combined with other drugs can ameliorate paraquat- or oleic acid-induced lung injury. However, the effect of OMT on lipopolysaccharide (LPS)-induced ALI remains unknown. The aim of the present study was to evaluate whether OMT can attenuate LPS-induced ALI through regulation of the ENaC and MAPK pathway using an ALI mouse model...
March 9, 2018: Experimental Animals
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
William J Zacharias, David B Frank, Jarod A Zepp, Michael P Morley, Farrah A Alkhaleel, Jun Kong, Su Zhou, Edward Cantu, Edward E Morrisey
Functional tissue regeneration is required for the restoration of normal organ homeostasis after severe injury. Some organs, such as the intestine, harbour active stem cells throughout homeostasis and regeneration; more quiescent organs, such as the lung, often contain facultative progenitor cells that are recruited after injury to participate in regeneration. Here we show that a Wnt-responsive alveolar epithelial progenitor (AEP) lineage within the alveolar type 2 cell population acts as a major facultative progenitor cell in the distal lung...
February 28, 2018: Nature
Michael F Nyp, Sherry M Mabry, Angels Navarro, Heather Menden, Ricardo E Perez, Venkatesh Sampath, Ikechukwu I Ekekezie
The onset and degree of injury occurring in animals that develop hyperoxic acute lung injury (HALI) is dependent on age at exposure, suggesting that developmentally regulated pathways/factors must underlie initiation of the epithelial injury and subsequent repair. Type II TGFβ receptor interacting protein-1 (TRIP-1) is a negative regulator of TGFβ signaling, which we have previously shown is a developmentally regulated protein with modulatory effects on epithelial-fibroblastic signaling. The aim of this study was to assess if type II alveolar epithelial cells overexpressing TRIP-1 are protected against hyperoxia-induced epithelial injury, and in turn HALI...
March 2018: Physiological Reports
Zhixi Li, Wenjun Jiang, Gang Wu, Xueming Ju, Youyu Wang, Wenying Liu
The identification and development of novel therapeutic strategies for acute lung injury is urgently required. It has been previously demonstrated that microRNA (miR)‑16 suppresses the level of transforming growth factor (TGF)‑β in acute lung injury (ALI). Therefore, the present study investigated the role of miR‑16 in the phenotype, cell proliferation and apoptosis, and the involvement of TGF‑β/Smad family member 2 (Smad2) and JAK/signal transducer and activator of transcription (STAT)3 signaling, of primary human alveolar type II epithelial cells (AECII)...
February 26, 2018: Molecular Medicine Reports
Martin S Taylor, Raghu R Chivukula, Laura C Myers, William R Jeck, Avinash Waghray, Purushothama R Tata, Martin K Selig, Walter J O'Donnell, Carol F Farver, B Taylor Thompson, Jayaraj Rajagopal, Richard L Kradin
Improved tools have led to a burgeoning understanding of lung regeneration in mice, but it is not yet known how these insights may be relevant to acute lung injury in humans. We report in detail two cases of fulminant idiopathic acute lung injury requiring extracorporeal membrane oxygenation in previously healthy young adults with acute respiratory distress syndrome, one of whom required lung transplantation. Biopsies showed diffuse alveolar injury with a striking paucity of alveolar epithelial regeneration, rare hyaline membranes, and diffuse contiguous airspace lining by macrophages...
February 21, 2018: American Journal of Pathology
Giacomo Sgalla, Bruno Iovene, Mariarosaria Calvello, Margherita Ori, Francesco Varone, Luca Richeldi
BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive disease characterized by the aberrant accumulation of fibrotic tissue in the lungs parenchyma, associated with significant morbidity and poor prognosis. This review will present the substantial advances achieved in the understanding of IPF pathogenesis and in the therapeutic options that can be offered to patients, and will address the issues regarding diagnosis and management that are still open. MAIN BODY: Over the last two decades much has been clarified about the pathogenic pathways underlying the development and progression of the lung scarring in IPF...
February 22, 2018: Respiratory Research
Li-Yin Hung, Taylor K Oniskey, Debasish Sen, Matthew F Krummel, Andrew E Vaughan, Noam A Cohen, De'Broski R Herbert
Trefoil factors are small secreted proteins that regulate tissue integrity and repair at mucosal surfaces, particularly in the gastrointestinal tract. However, their relative contribution(s) to controlling baseline lung function or the extent of infection-induced lung injury are unknown issues. Using irradiation bone marrow chimeras, we found that Trefoil factor 2 (TFF2) produced from both hematopoietic- and non-hematopoietic-derived cells is essential for host protection, proliferation of alveolar type 2 cells, and restoration of pulmonary gas exchange following infection with the hookworm parasite Nippostrongylus brasiliensis...
February 16, 2018: American Journal of Pathology
Xiao Chen, Hailing Wang, Kui Jia, Hao Wang, Tao Ren
Pulmonary inflammation is a primary characteristic of lung injury initiated by the accession of immune cells into the alveolar space. Neutrophil migration serves an important role in pulmonary inflammation mediated by the migration of neutrophils into hypoxic tissue sites. The elimination of pulmonary inflammation is directly associated with rehabilitation in patients with lung injury. Anti-inflammatory treatment is essential following lung injury and ultimately determines patient outcomes. Semaphorin-7A (SEMA-7A) is a member of the Semaphorin family that influences the migration of neutrophils into hypoxic tissue sites, thus promoting inflammation...
March 2018: Experimental and Therapeutic Medicine
Masashi Kawami, Rika Harabayashi, Risako Harada, Yohei Yamagami, Ryoko Yumoto, Mikihisa Takano
Methotrexate (MTX) often induces serious lung diseases such as pulmonary fibrosis. Although MTX is known to be a folic acid (FA) antagonist, the effect of FA on MTX-induced lung injury remains unclear. Recent studies indicate that epithelial-mesenchymal transition (EMT) is involved in pulmonary fibrosis. Here, we aimed to clarify the effect of FA on MTX-induced EMT in human alveolar epithelial cell line A549 using conditioned medium (CM). CM was prepared from the supernatants of A549 cells treated with MTX in the absence (CMM) or presence (CMMF) of FA...
February 12, 2018: Biochemical and Biophysical Research Communications
Charles A Downs, Nicholle M Johnson, George Tsaprailis, My N Helms
The receptor for advanced glycation end-products (RAGE) is a pattern recognition receptor and member of the immunoglobulin superfamily. RAGE is constitutively expressed in the distal lung where it co-localizes with the alveolar epithelium; RAGE expression is otherwise minimal or absent, except with disease. This suggests RAGE plays a role in lung physiology and pathology. We used proteomics to identify and characterize the effects of RAGE on rat alveolar epithelial (R3/1) cells. LC-MS/MS identified 177 differentially expressed proteins and the PANTHER Classification System further segregated proteins...
February 12, 2018: Journal of Proteomics
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
Song Qin, Miao Chen, Hui Ji, Guo-Yue Liu, Hong Mei, Kang Li, Tao Chen
Hyperoxia‑induced acute lung injury (HALI) as one of the most common complications in patents on mechanical ventilation, and there are no efficient methods to overcome this at present. It was hypothesized that microRNA 21‑5p(miR‑21‑5p) can promote the survival of type II alveolar epithelial cells (AECII), alleviating HALI. The present study aimed to combine gene chip analysis with the overexpression miR‑21‑5p to develop a novel therapeutic option for HALI. It was found that AECII apoptosis was an important pathogenic event in the development of HALI, and the overexpression of miR‑21‑5p prevented HALI, associated with reducing AECII apoptosis...
February 6, 2018: Molecular Medicine Reports
Peng-Cheng Li, Bo-Rong Wang, Cong-Cong Li, Xi Lu, Wei-Sheng Qian, Yu-Juan Li, Fa-Guang Jin, De-Guang Mu
Seawater (SW) inhalation can induce acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). In the present study, SW induced apoptosis of rat alveolar epithelial cells and histopathological alterations to lung tissue. Furthermore, SW administration increased generation of reactive oxygen species (ROS), whereas pretreatment with the ROS scavenger, N‑acetyl‑L‑cysteine (NAC), significantly decreased ROS generation, apoptosis and histopathological alterations. In addition, SW exposure upregulated the expression levels of glucose‑regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP), which are critical proteins in the endoplasmic reticulum (ER) stress response, thus indicating that SW may activate ER stress...
February 12, 2018: International Journal of Molecular Medicine
Jinfeng Liu, Wei Wang, Fengli Liu, Zhenguang Li
Acute respiratory distress syndrome (ARDS) mainly involves acute respiratory failure. In addition to this affected patients feel progressive arterial hypoxemia, dyspnea, and a marked increase in the work of breathing. The only clinical solution for the above pathological state is ventilation. Mechanical ventilation is necessary to support life in ARDs but it itself worsen lung injury and the term is known clinically as 'ventilation induced lung injury' (VILI). At the cellular level, respiratory epithelial cells are subjected to cyclic stretch, i...
February 2018: Experimental and Therapeutic Medicine
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