scholarly journals Type I interferon promotes alveolar epithelial type II cell survival during pulmonary Streptococcus pneumoniae infection and sterile lung injury in mice

2016 ◽  
Vol 46 (9) ◽  
pp. 2175-2186 ◽  
Author(s):  
Barbara B. Maier ◽  
Anastasiya Hladik ◽  
Karin Lakovits ◽  
Ana Korosec ◽  
Rui Martins ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Lung Injury ◽  
Cell Survival ◽  
Type I Interferon ◽  
Type I ◽  
Type Ii ◽  
Alveolar Epithelial ◽  
Type Ii Cell

Late Breaking Abstract - Aging impairs alveolar epithelial type II cell function in acute lung injury

2019 ◽  
Author(s):  
Christina Brandenberger ◽  
Tolga Yazicioglu ◽  
Cheng-Kai Huang ◽  
Christian Bär ◽  
Christian Mühlfeld
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Cell Function ◽  
Type Ii ◽  
Alveolar Epithelial ◽  
Type Ii Cell

Aging causes alveolar epithelial type II cell dysfunction in acute lung injury

2020 ◽  
Author(s):  
C Brandenberger ◽  
T Yazicioglu ◽  
C Autilio ◽  
C Huang ◽  
C Bär ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Type Ii ◽  
Alveolar Epithelial ◽  
Cell Dysfunction ◽  
Type Ii Cell

scholarly journals Alveolar Epithelial Type II Cell Function in Acute Lung Injury Is Impaired in Old Mice

2020 ◽  
Author(s):  
C. Brandenberger ◽  
T. Yazicioglu ◽  
C. Autilio ◽  
C.-K. Huang ◽  
C. Bär ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Cell Function ◽  
Type Ii ◽  
Alveolar Epithelial ◽  
Type Ii Cell ◽  
Old Mice

Hyperoxia increases keratinocyte growth factor mRNA expression in neonatal rabbit lung

1999 ◽  
Vol 276 (1) ◽  
pp. L105-L113 ◽  
Author(s):  
Lama Charafeddine ◽  
Carl T. D’Angio ◽  
Julie L. Richards ◽  
Barry R. Stripp ◽  
Jacob N. Finkelstein ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Lung Injury ◽  
Mrna Expression ◽  
Keratinocyte Growth Factor ◽  
Nuclear Antigen ◽  
Type Ii ◽  
Alveolar Epithelial ◽  
Hyperoxic Lung Injury ◽  
Type Ii Cell ◽  
Proliferating Cell

Acute hyperoxic lung injury remains a major factor in the development of chronic lung disease in neonates. A critical step in the repair of acute lung injury is the proliferation of type II alveolar epithelial cells. Type II cell proliferation is stimulated by keratinocyte growth factor (KGF), an epithelial cell-specific mitogen. We sought to investigate KGF mRNA expression in relation to type II cell proliferation during hyperoxic lung injury. We studied a previously described newborn (NB) rabbit model of acute and chronic hyperoxic injury [C. T. D’Angio, J. N. Finkelstein, M. B. LoMonaco, A. Paxhia, S. A. Wright, R. B. Baggs, R. H. Notter, and R. M. Ryan. Am. J. Physiol. 272 ( Lung Cell. Mol. Physiol. 16): L720–L730, 1997]. NB rabbits were placed in 100% O2 for 9 days and then recovered in 60% O2. RT-PCR was used to synthesize and amplify a 267-bp fragment of rabbit KGF cDNA from whole lung RNA. KGF mRNA expression was analyzed by ribonuclease protection assay, and mRNA abundance was quantified by phosphorimaging. Proliferating cell nuclear antigen immunohistochemistry was used on lung sections to identify proliferating cells. The rabbit partial cDNA sequenced was >95% homologous to human cDNA, and all amino acids were conserved. Whole lung KGF mRNA expression was increased 12-fold after 6 days of hyperoxia compared with control lungs, and remained increased throughout the 100% O2 exposure period. Proliferating cell nuclear antigen immunohistochemistry showed an increase in type II cell proliferation after 8–12 days of hyperoxia. NB rabbits exposed to hyperoxic injury exhibit increased whole lung KGF mRNA expression preceding type II cell proliferation. KGF may be an important mitogen in the regulation of alveolar epithelial repair after hyperoxic lung injury.

Augmented expression of cytosolic phospholipase A2 during phenotypic transformation of cultured type II pneumocytes

1994 ◽  
Vol 266 (2) ◽  
pp. C382-C390 ◽  
Author(s):  
M. Peters-Golden ◽  
A. Feyssa
Keyword(s):  
Phospholipase A2 ◽  
Molecular Mass ◽  
Immunoblot Analysis ◽  
Alveolar Epithelial Cells ◽  
Cell Phenotype ◽  
Type I ◽  
Type Ii ◽  
Alveolar Epithelial ◽  
Type Ii Pneumocytes ◽  
Type Ii Cell

Over time in culture, rat type II alveolar epithelial cells (AEC) demonstrate increased levels of unesterified arachidonic acid (AA) and increased prostanoid synthesis, while assuming certain morphological and biochemical characteristics of the type I cell phenotype. The objective of this study was to elucidate the enzymatic mechanism(s) responsible for increased AA accumulation in this model. Cells were examined both early in culture (2 days), when they retained type II cell features, and later in culture (7 days), when they are known to express a number of type I cell characteristics. An increase in AA levels at day 7 persisted despite inhibition of AA reacylation, suggesting that differences in deacylation were responsible for differences in free fatty acid levels. These differences in deacylation were not explained by differing susceptibilities to hydrolysis of radiolabeled endogenous lipids from day 2 and day 7 cells. The phospholipase A2 (PLA2) activities at both days in culture were qualitatively similar and typical of the recently described high-molecular-mass cytosolic PLA2 (cPLA2), but activity in day 7 cytosol was threefold greater than that present in day 2 cytosol. A neutralizing anti-cPLA2 antibody reduced the PLA2 activity in day 7 cytosol to the level found in day 2 cytosol. Immunoblot analysis failed to detect expression of low-molecular-mass PLA2 proteins but confirmed that expression of the 97-kDa cPLA2 was greater in day 7 cytosol than in day 2 cytosol. These results indicate that increased levels of unesterified AA in AEC with phenotype altered during culture are due to augmented steady-state expression of cPLA2 and suggest for the first time that expression of cPLA2 is differentiation dependent.

scholarly journals Generation of an alveolar epithelial type II cell line from induced pluripotent stem cells

2018 ◽  
Vol 315 (6) ◽  
pp. L921-L932 ◽  
Author(s):  
Luca Tamò ◽  
Youssef Hibaoui ◽  
Sampada Kallol ◽  
Marco P. Alves ◽  
Christiane Albrecht ◽  
...  
Keyword(s):  
Cell Line ◽  
Cell Biology ◽  
Alveolar Epithelial Cell ◽  
Surfactant Protein ◽  
Type I ◽  
Type Ii ◽  
Alveolar Epithelial ◽  
Type Ii Cell ◽  
Induced Pluripotent

Differentiation of primary alveolar type II epithelial cells (AEC II) to AEC type I in culture is a major barrier in the study of the alveolar epithelium in vitro. The establishment of an AEC II cell line derived from induced pluripotent stem cells (iPSC) represents a novel opportunity to study alveolar epithelial cell biology, for instance, in the context of lung injury, fibrosis, and repair. In the present study, we generated long-lasting AEC II from iPSC (LL-iPSC-AEC II). LL-iPSC-AEC II displayed morphological characteristics of AEC II, including growth in a cobblestone monolayer, the presence of lamellar bodies, and microvilli, as shown by electron microscopy. Also, LL-iPSC-AEC II expressed AEC type II proteins, such as cytokeratin, surfactant protein C, and LysoTracker DND 26 (a marker for lamellar bodies). Furthermore, the LL-iPSC-AEC II exhibited functional properties of AEC II by an increase of transepithelial electrical resistance over time, secretion of inflammatory mediators in biologically relevant quantities (IL-6 and IL-8), and efficient in vitro alveolar epithelial wound repair. Consistent with the AEC II phenotype, the cell line showed the ability to uptake and release surfactant protein B, to secrete phospholipids, and to differentiate into AEC type I. In summary, we established a long-lasting, but finite AEC type II cell line derived from iPSC as a novel cellular model to study alveolar epithelial cell biology in lung health and disease.

scholarly journals The History and Mystery of Alveolar Epithelial Type II Cells: Focus on Their Physiologic and Pathologic Role in Lung

2021 ◽  
Vol 22 (5) ◽  
pp. 2566 ◽  
Author(s):  
Barbara Ruaro ◽  
Francesco Salton ◽  
Luca Braga ◽  
Barbara Wade ◽  
Paola Confalonieri ◽  
...  
Keyword(s):  
Host Defense ◽  
Defense Mechanisms ◽  
Work Of Breathing ◽  
Surfactant Proteins ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii ◽  
Lung Protection ◽  
Alveolar Epithelial ◽  
Distal Lung

Alveolar type II (ATII) cells are a key structure of the distal lung epithelium, where they exert their innate immune response and serve as progenitors of alveolar type I (ATI) cells, contributing to alveolar epithelial repair and regeneration. In the healthy lung, ATII cells coordinate the host defense mechanisms, not only generating a restrictive alveolar epithelial barrier, but also orchestrating host defense mechanisms and secreting surfactant proteins, which are important in lung protection against pathogen exposure. Moreover, surfactant proteins help to maintain homeostasis in the distal lung and reduce surface tension at the pulmonary air–liquid interface, thereby preventing atelectasis and reducing the work of breathing. ATII cells may also contribute to the fibroproliferative reaction by secreting growth factors and proinflammatory molecules after damage. Indeed, various acute and chronic diseases are associated with intensive inflammation. These include oedema, acute respiratory distress syndrome, fibrosis and numerous interstitial lung diseases, and are characterized by hyperplastic ATII cells which are considered an essential part of the epithelialization process and, consequently, wound healing. The aim of this review is that of revising the physiologic and pathologic role ATII cells play in pulmonary diseases, as, despite what has been learnt in the last few decades of research, the origin, phenotypic regulation and crosstalk of these cells still remain, in part, a mystery.

scholarly journals β-Catenin/Lin28/let-7 regulatory network determines type II alveolar epithelial stem cell differentiation phenotypes following thoracic irradiation

2020 ◽  
Vol 62 (1) ◽  
pp. 119-132
Author(s):  
Xiaozhuan Liu ◽  
Tingting Zhang ◽  
Jianwei Zhou ◽  
Ziting Xiao ◽  
Yanjun Li ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Stem Cell Differentiation ◽  
Alveolar Epithelial Cells ◽  
Type I ◽  
Type Ii ◽  
Epithelial Stem Cells ◽  
Alveolar Epithelial ◽  
Thoracic Irradiation ◽  
Radiation Induced ◽  
Differentiation Marker

Abstract The contribution of type II alveolar epithelial stem cells (AEC II) to radiation-induced lung fibrosis (RILF) is largely unknown. Cell differentiation phenotypes are determined by the balance between Lin28 and lethal-7 microRNA (let-7 miRNA). Lin28 is activated by β-catenin. The aim of this study was to track AEC II phenotypes at different phases of injury following thoracic irradiation and examine the expression of β-catenin, Lin28 and let-7 to identify their role in AEC II differentiation. Results showed that coexpression of prosurfactant protein C (proSP-C, an AEC II biomarker) and HOPX (homeobox only protein X, an AEC I biomarker) or vimentin (a differentiation marker) was detected in AEC II post-irradiation. The protein expression levels of HOPX and proSP-C were significantly downregulated, but vimentin was significantly upregulated following irradiation. The expression of E-cadherin, which prevents β-catenin from translocating to the nucleus, was downregulated, and the expression of β-catenin and Lin28 was upregulated after irradiation (P < 0.05 to P < 0.001). Four let-7 miRNA members (a, b, c and d) were upregulated in irradiated lungs (P < 0.05 to P < 0.001), but let-7d was significantly downregulated at 5 and 6 months (P < 0.001). The ratios of Lin28 to four let-7 members were low during the early phase of injury and were slightly higher after 2 months. Intriguingly, the Lin28/let-7d ratio was strikingly increased after 4 months. We concluded that β-catenin contributed to RILF by promoting Lin28 expression, which increased the number of AEC II and the transcription of profibrotic molecules. In this study, the downregulation of let-7d miRNA by Lin28 resulted in the inability of AEC II to differentiate into type I alveolar epithelial cells (AEC I).

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