Relevant bibliographies by topics / Alveolar type cell

Academic literature on the topic 'Alveolar type cell'

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Published: 1 April 2023

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Journal articles on the topic "Alveolar type cell"

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Chen, Qian, Varsha Suresh Kumar, Johanna Finn, Dianhua Jiang, Jiurong Liang, You-yang Zhao, and Yuru Liu. "CD44high alveolar type II cells show stem cell properties during steady-state alveolar homeostasis." American Journal of Physiology-Lung Cellular and Molecular Physiology 313, no. 1 (July 1, 2017): L41—L51. http://dx.doi.org/10.1152/ajplung.00564.2016.

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The alveolar epithelium is composed of type I cells covering most of the gas-blood exchange surface and type II cells secreting surfactant that lowers surface tension of alveoli to prevent alveolar collapse. Here, we have identified a subgroup of type II cells expressing a higher level of cell surface molecule CD44 (CD44high type II cells) that composed ~3% of total type II cells in 5–10-wk-old mice. These cells were preferentially apposed to lung capillaries. They displayed a higher proliferation rate and augmented differentiation capacity into type I cells and the ability to form alveolar organoids compared with CD44low type II cells. Moreover, in aged mice, 18–24 mo old, the percentage of CD44high type II cells among all type II cells was increased, but these cells showed decreased progenitor properties. Thus CD44high type II cells likely represent a type II cell subpopulation important for constitutive regulation of alveolar homeostasis.
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Wang, P. M., E. Fujita, and J. Bhattacharya. "Vascular regulation of type II cell exocytosis." American Journal of Physiology-Lung Cellular and Molecular Physiology 282, no. 5 (May 1, 2002): L912—L916. http://dx.doi.org/10.1152/ajplung.00303.2001.

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To determine whether lung capillary pressure regulates surfactant secretion, we viewed alveoli of the constantly inflated, isolated blood-perfused rat lung by fluorescence microscopy. By alveolar micropuncture we infused fura 2 and lamellar body (LB)-localizing dyes for fluorescence detection of, respectively, the alveolar cytosolic Ca2+concentration ([Ca2+]i) and type II cell exocytosis. Increasing left atrial pressure (Pla) from 5 to 10 cmH2O increased septal capillary diameter by 26% and induced marked alveolar [Ca2+]i oscillations that abated on relief of pressure elevation. The rate of loss of LB fluorescence that reflects the LB exocytosis rate increased fourfold after the pressure elevation and continued at the same rate even after pressure and [Ca2+]i oscillations had returned to baseline. In alveoli pretreated with either 1,2-bis(2-aminophenoxy)ethane- N,N,N′,N′-tetraacetic acid-AM, the intracellular Ca2+ chelator, or heptanol, the gap junctional blocker, the pressure-induced exocytosis was completely inhibited. We conclude that capillary pressure and surfactant secretion are mechanically coupled. The secretion initiates in a Ca2+-dependent manner but is sustained by Ca2+-independent mechanisms.
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Sutherland, Leanne M., Yasmin S. Edwards, and Andrew W. Murray. "Alveolar type II cell apoptosis." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 129, no. 1 (May 2001): 267–85. http://dx.doi.org/10.1016/s1095-6433(01)00323-3.

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Dormans, J. A. M. A. "The alveolar type III cell." Lung 163, no. 1 (December 1985): 327–35. http://dx.doi.org/10.1007/bf02713833.

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Hall, Joshua D., Robin R. Craven, James R. Fuller, Raymond J. Pickles, and Thomas H. Kawula. "Francisella tularensis Replicates within Alveolar Type II Epithelial Cells In Vitro and In Vivo following Inhalation." Infection and Immunity 75, no. 2 (November 6, 2006): 1034–39. http://dx.doi.org/10.1128/iai.01254-06.

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ABSTRACT Francisella tularensis replicates in macrophages and dendritic cells, but interactions with other cell types have not been well described. F. tularensis LVS invaded and replicated within alveolar epithelial cell lines. Following intranasal inoculation of C57BL/6 mice, Francisella localized to the alveolus and replicated within alveolar type II epithelial cells.
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Wang, Yanjie, Zan Tang, Huanwei Huang, Jiao Li, Zheng Wang, Yuanyuan Yu, Chengwei Zhang, et al. "Pulmonary alveolar type I cell population consists of two distinct subtypes that differ in cell fate." Proceedings of the National Academy of Sciences 115, no. 10 (February 20, 2018): 2407–12. http://dx.doi.org/10.1073/pnas.1719474115.

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Pulmonary alveolar type I (AT1) cells cover more than 95% of alveolar surface and are essential for the air–blood barrier function of lungs. AT1 cells have been shown to retain developmental plasticity during alveolar regeneration. However, the development and heterogeneity of AT1 cells remain largely unknown. Here, we conducted a single-cell RNA-seq analysis to characterize postnatal AT1 cell development and identified insulin-like growth factor-binding protein 2 (Igfbp2) as a genetic marker specifically expressed in postnatal AT1 cells. The portion of AT1 cells expressing Igfbp2 increases during alveologenesis and in post pneumonectomy (PNX) newly formed alveoli. We found that the adult AT1 cell population contains both Hopx+Igfbp2+ and Hopx+Igfbp2− AT1 cells, which have distinct cell fates during alveolar regeneration. Using an Igfbp2-CreER mouse model, we demonstrate that Hopx+Igfbp2+ AT1 cells represent terminally differentiated AT1 cells that are not able to transdifferentiate into AT2 cells during post-PNX alveolar regeneration. Our study provides tools and insights that will guide future investigations into the molecular and cellular mechanism or mechanisms underlying AT1 cell fate during lung development and regeneration.
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Rybicka, Krystyna. "Histogenesis of alveolar cell carcinoma." Proceedings, annual meeting, Electron Microscopy Society of America 45 (August 1987): 626–27. http://dx.doi.org/10.1017/s0424820100127566.

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Alveolar cell carcinoma (ACC) is a lung neoplasm characterized by the presence of lamellar bodies specific for normal type 2 alveolar cells. Tumor histogenesis is uncertain. The present study indicates that ACC originates from dedifferentiation of hyperplastic type 2 alveolar cells rather than migration of bronchial stem cells into alveoli as suggested earlier.An aliquot of human lung biopsy diagnosed as ACC was fixed in glutaraldehyde and osmium, treated with 1% aqueous uranyl acetate, and embedded in epoxy resin. Sections were stained for glycogen by periodic acid - thiosemicarbazide - silver proteinate, and post-stained by uranyl acetate and lead citrate.The tumor contained morphologically distinct cell clusters. Each cluster consisted of identical cells. Differences between clusters resulted from synchronous alterations in lamellar bodies, mitochondria, glycosomes, and ribosomes. These alterations revealed distinct stages in cell differentiation classified here as follows: stage 1-hyperplastic cells (Fig.1), stage 2-dedifferentiating cells (Fig.2), stage 3-undifferentiated cells (Fig.3), stage 4-differentiating cells (Fig.4).
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Ichimura, Hideo, Kaushik Parthasarathi, Jens Lindert, and Jahar Bhattacharya. "Lung surfactant secretion by interalveolar Ca2+ signaling." American Journal of Physiology-Lung Cellular and Molecular Physiology 291, no. 4 (October 2006): L596—L601. http://dx.doi.org/10.1152/ajplung.00036.2006.

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Although clusters of alveoli form the acinus, which is the most distal respiratory unit, it is not known whether interalveolar communication coordinates acinar surfactant secretion. To address this, we applied real-time digital imaging in conjunction with photo-excited Ca2+ uncaging in intact alveoli of the isolated, blood-perfused rat lung. We loaded alveolar cells with the Ca2+ cage o-nitrophenyl EGTA-AM (NP-EGTA-AM) together with the fluorophores, fluo 4, or LysoTracker green (LTG) to determine, respectively, the cytosolic Ca2+ concentration ([Ca2+]cyt) or type 2 cell secretion. To uncage Ca2+ from NP-EGTA, we exposed a region in a selected alveolus to high-intensity UV illumination. As a result, fluo 4 fluorescence increased, whereas LTG fluorescence decreased, in the photo-targeted region, indicating that uncaging both increased [Ca2+]cyt and induced secretion. Concomitantly, [Ca2+]cyt increases conducted from the uncaging site induced type 2 cell secretion in both the selected alveolus as well as in neighboring alveoli, indicating the presence of interalveolar communication. These conducted responses were inhibited by pretreating alveoli with the connexin43 (Cx43)-inhibiting peptides gap 26 and gap 27. However, although the conducted [Ca2+]cyt increase diminished with distance from the uncaging site, type 2 cell secretion rates were similar at all locations. We conclude that Cx43-dependent, interalveolar Ca2+ signals regulate type 2 cell secretion in adjacent alveoli. Such interalveolar communication might facilitate acinar coordination of alveolar function.
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Cott, G. R., K. Sugahara, and R. J. Mason. "Stimulation of net active ion transport across alveolar type II cell monolayers." American Journal of Physiology-Cell Physiology 250, no. 2 (February 1, 1986): C222—C227. http://dx.doi.org/10.1152/ajpcell.1986.250.2.c222.

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The active transcellular transport of electrolytes across the alveolar epithelium probably plays an important role in alveolar fluid homeostasis by helping to maintain the alveolus relatively free of fluid. To better understand the factors regulating active ion transport across alveolar epithelial cells, we examined the effect of a number of pharmacologically active agents on the bioelectric properties of alveolar type II cells in primary culture. Alveolar type II cells were isolated from adult male rats and cultured on collagen-coated Millipore filters for 6-14 days. The bioelectric properties of these monolayers were determined in Ussing-type chambers. The addition of 10(-3) M 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP) increased the short-circuit current (Isc) from 2.9 +/- 0.75 to 6.9 +/- 0.73 microA/cm2 (means +/- SE; n = 8) and decreased the transepithelial resistance. Cholera toxin, 3-isobutyl-1-methylxanthine, and terbutaline sulfate produced similar increases in Isc and decreases in resistance. The Isc stimulated by 8-BrcAMP was Na but not Cl dependent and could be blocked by amiloride but not by furosemide. Thus 8-BrcAMP and agents that increase intracellular cAMP can stimulate a Na-dependent net active ion transport across alveolar type II cell monolayers. Similar regulatory mechanisms may be involved in controlling solute and fluid movement across the alveolar epithelium in vivo.
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Parra, Saundra C., Ricky Burnette, and Timothy Takaro. "Computer Reconstructions of Normal Human Alveoli From Serial Sections." Proceedings, annual meeting, Electron Microscopy Society of America 43 (August 1985): 312–13. http://dx.doi.org/10.1017/s0424820100118436.

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Portions of two adjacent normal human alveoli were reconstructed from serial sections in order to examine normal alveolar organization, including anatomical relationships among the different cell types, the connective tissue matrix and gaps in the alveolar septum. Computer reconstructions were prepared from montaged electron micrographs of serial sections. Rotation of these reconstructions in the x, y or z axes allowed examination of the alveoli from many different aspects other than the actual plane of sectioning. Anatomical relationships “between Type I and Type II epithelial cells, alveolar macrophages, and pores of Kohn that could not he deduced from a single plane of the section (random sections) were revealed.
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Dissertations / Theses on the topic "Alveolar type cell"

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Bhandari, R. N. B. "Characterization of a cell adhesion receptor on rat lung alveolar type 2 cells." Thesis, Imperial College London, 1988. http://hdl.handle.net/10044/1/46962.

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Hofer, Christian Carlisle. "Effects of Influenza Infection on Murine Alveolar Type II Cell Function." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1406201295.

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Hasegawa, Kouichi. "Fraction of MHCII and EpCAM expression characterizes distal lung epithelial cells for alveolar type 2 cell isolation." Kyoto University, 2018. http://hdl.handle.net/2433/232118.

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Downs, Charles. "Cigarette Smoke Extract-Induced Injury in Alveolar Cells in Model Systems." Diss., The University of Arizona, 2011. http://hdl.handle.net/10150/201510.

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Cigarette smoke contributes to many diseases. The actions of second and third hand smoke, which have implications for non-smokers and the very young, are just beginning to be appreciated. The overarching hypothesis of this project is that cigarette smoke has different injurious actions on alveolar cells based on chronological age. The purpose here was to learn more about the susceptibility of alveolar cells to cigarette smoke extract (CSE)- induced injury by performing studies on pulmonary alveolar and endothelial cells derived from neonatal, young, and old rats. The aims involved: 1. Developing cell culture models to study age-related effects of cigarette smoke on alveolar type I cells and microvascular endothelial cells from the lung, and 2. Using these models to examine the effects of CSE on markers of oxidative stress, inflammation and aging in alveolar cells harvested from neonatal, young and old rats. Descriptive and experimental studies involved using a variety of cell culture, biochemical and molecular techniques, including gene expression arrays. The most significant findings were that: 1. primary proliferating alveolar type I cells were used to develop novel cell culture model systems, including single culture, co-culture and three-dimensional cultures that were used to study the effects of CSE; 2. Hydrogen peroxide production by endothelial cells was markedly reduced by co-culturing with AT I cells; 3. Gene expression profiling of oxidative stress-specific pathways suggest that genes responsible for both stopping production of H2O2 or mopping-up H2O2 are involved; and 4. Cigarette smoke shortens telomeres of cells from neonates, but unexpectedly preserves telomere length of cells from young and old rats. Data from telomeric pathway-specific gene expression arrays suggest that there are age-related differences in response to gene expression to CSE. The significant conclusions are: 1. Contrary to prior observations, alveolar type I cells demonstrate prolonged proliferative capacity; 2. Alveolar type I cells likely play an important role in ameliorating CSE-induced oxidative stress; and 3. Neonatal alveolar cells may be more susceptible to the deleterious effects of CSE including telomere shortening. These novel model systems and observations provide new ways to study cigarette smoke-associated lung dysfunction.
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Downs, Charles A., Abdel A. Alli, Nicholle M. Johnson, and My N. Helms. "Cigarette smoke extract is a Nox agonist and regulates ENaC in alveolar type 2 cells." AMER INST MATHEMATICAL SCIENCES-AIMS, 2016. http://hdl.handle.net/10150/621494.

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There is considerable evidence that cigarette smoking is the primary etiology of chronic obstructive pulmonary disease (COPD), and that oxidative stress occurs in COPD with the family of tissue nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Nox) enzymes playing a significant role in lung pathogenesis. The purpose of this study was to determine the effects of cigarette smoke extract (CSE) on Nox signaling to epithelial sodium channels (ENaCs). Pre-treatment with diphenyleneiodonium (DPI), a pan-Nox inhibitor, prevented stimulatory effects of CSE on ENaC activity; open probability (Po) changed from 0.36 +/- 0.09 to 0.11 +/- 0.02; n=10, p=0.01 following CSE and DPI exposure. Likewise, Fulvene-5 (which inhibits Nox2 and Nox4 isoforms) decreased the number of ENaC per patch (from 2.75 +/- 0.25 to 1 +/- 0.5, n=9, p=0.002) and open probability (0.18 +/- 0.08 to 0.02 +/- 0.08, p=0.04). Cycloheximide chase assays show that CSE exposure prevented alpha-ENaC subunit degradation, whereas concurrent CSE exposure in the presence of Nox inhibitor, Fulvene 5, resulted in normal proteolytic degradation of alpha-ENaC protein in primary isolated lung cells. In vivo, co-instillation of CSE and Nox inhibitor promoted alveolar flooding in C57Bl6 mice compared to accelerated rates of fluid clearance observed in CSE alone instilled lungs. Real-time PCR indicates that mRNA levels of Nox2 were unaffected by CSE treatment while Nox4 transcript levels significantly increased 3.5 fold in response to CSE. Data indicate that CSE is an agonist of Nox4 enzymatic activity, and that CSE-mediated Nox4 plays an important role in altering lung ENaC activity.
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Clegg, Gareth Roger. "Co-expression of lung alveolar epithelial type I and II cell-selective proteins in response to injury." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/29066.

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This study used a novel combination of ATI and ATII cell-selective antibodies to investigate the phenotype of the alveolar epithelium following Staphylococcus aureus-induced ‘direct’ lung injury.   Following distal airway instillation of S. aureus, the alveolar epithelium was covered with ATII cells (MMC4/RTII70-positive cells) and ATI cells (RTI40-positive cells) as seen in control lungs. However, the surface area covered by ATII cells was significantly increased, while the surface area covered by ATI cells was significantly decreased, in comparison with controls. The alveolar wall of S. aureus-injured lungs also contained cells that co-stained-with a unique combination of ATI and ATII cell proteins, RTI40 and MMC4. To determine whether RTI40/MMC4-positive cells were likely to be intermediates in the transition of ATII to ATI cells I examined ATII cells as they transformed to ATI-like cells in culture (day 0 to 5). Only cells on day 1 of culture were RTI40/MMC4 positive. I also examined the developing lung for RT140/MC40 positive cells. Co-staining cells were not found in the developing alveolar epithelium, but they were present in small airways. I also developed a rat model of haemorrhagic shock induced ‘indirect’ alveolar epithelial injury as a platform for future work. Here I have developed a robust technique for imaging ATII cell transdifferentiation in vivo and in vitro. This work has identified a novel alveolar epithelial phenotype, RTI40/MMC4, in repairing lungs and in ATII cells as they transdifferentiate to ATI-like cells in vitro. These data suggest that RTI40/MMC4-positive cells can be used to both visualise alveolar epithelial intermediates in vivo and to investigate the regulation of ATII cell transdifferentiation following injury.
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Korogi, Yohei. "In Vitro Disease Modeling of Hermansky-Pudlak Syndrome Type 2 Using Human Induced Pluripotent Stem Cell-Derived Alveolar Organoids." Kyoto University, 2019. http://hdl.handle.net/2433/243303.

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Dysart, Marilyn Markowski. "Remodeling of the pulmonary microenvironment controls transforming growth factor-beta activation and alveolar type II epithelial to mesenchymal transition." Diss., Georgia Institute of Technology, 2014. http://hdl.handle.net/1853/53421.

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Pulmonary fibrosis is a potentially deadly pathology characterized by excessive deposition of extracellular matrix (ECM), increased tissue stiffness, and loss of tissue structure and function. Recent evidence has suggested epithelial to mesenchymal transition (EMT), the transdifferentiation of an epithelial cell into a mesenchymal fibroblast, is one mechanism that results in the accumulation of myofibroblasts and excessive deposition of ECM. EMT is a highly orchestrated process involving the integration of biochemical signals from specific integrin mediated interactions with ECM proteins and soluble growth factors including TGFβ. TGFβ, a potent inducer of EMT, can be activated by cell contraction mediated mechanical release of the growth factor from a macromolecular latent complex. Therefore, TGFβ activity and subsequent EMT may be influenced by both the biochemical composition and biophysical state of the surrounding ECM. Based on these knowns it was first investigated how changes in the biochemical composition of the matrix and changes in tissue rigidity together modulate EMT due to changes in epithelial cell contraction and TGFβ activation. Here we show that integrin specific interactions with fibronectin (Fn) variants displaying both the RGD and PHSRN binding sites facilitate cell binding through α3β1 and α5β1 integrins, and that these interactions maintain an epithelial phenotype despite engagement of increased tissue rigidities. Conversely, Fn fragments that facilitate cell binding through αv integrins drive TGFβ activation and subsequent EMT even while engaging soft underlying substrates. Adding to the complexity of studying mechanisms that contribute to pulmonary fibrosis, is exposure of the lung to injuries from environmental particulates. Therefore, we investigated how EMT is altered in response to particulate matter (PM). Here we show that PM exposure further drives TGFβ activation, EMT, and increases intracellular levels of reactive oxygen species (ROS). Additionally, cells binding the ECM through α5β1 and α3β1 integrins only partially recover an epithelial phenotype, suggesting ROS may be a secondary driver of TGFβ and EMT. Taken together these results suggest dynamic changes to the ECM microenvironment are major contributors to the control of EMT responses and provide insights into the design of biomaterial-based microenvironments for control of epithelial cell phenotype.
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Doolittle, Lauren May. "The Impact of Alveolar Type II Cell Mitochondrial Damage and Altered Energy Production on Acute Respiratory Distress Syndrome Development During Influenza A Virus Infection." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu159224389333959.

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Assis, Adriano Freitas de. "Desenvolvimento do fenótipo osteoblástico em células derivadas de osso alveolar humano cultivadas sobre titânio revestido com colágeno tipo I." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/58/58136/tde-30062008-140042/.

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Os eventos celulares e extracelulares que ocorrem durante o processo de osseointegração do titânio (Ti) são bastante influenciados por suas propriedades de superfície, como morfologia, topografia e composição química. A modificação bioquímica da superfície do Ti consiste em imobilizar proteínas ou peptídeos nessa superfície com a finalidade de induzir respostas celulares e teciduais específicas na interface osso-implante que acelerem ou aumentem a osseointegração. O objetivo deste estudo foi avaliar o desenvolvimento do fenótipo osteoblástico em culturas de células crescidas sobre Ti revestido com colágeno tipo I. Para tanto, células osteoblásticas derivadas de fragmentos ósseos do processo alveolar de humanos foram cultivadas sobre discos de Ti usinados revestidos (Ti-col) ou não (Ti-usinado) com colágeno tipo I e foram avaliados os seguintes parâmetros: adesão, morfologia e proliferação celulares, síntese de proteína total, atividade de fosfatase alcalina (ALP), formação de matriz mineralizada, e expressão de genes marcadores do fenótipo osteoblástico por reação em cadeia da polimerase em tempo real (PCR em tempo real). O Ti-col alterou o crescimento e a expressão gênica das culturas e não teve efeito na adesão e morfologia celulares, síntese de proteína total, atividade de ALP e formação de matriz mineralizada comparado ao Ti-usinado. Esses resultados indicam que a superfície Ti-col pode favorecer um maior crescimento da cultura durante a fase proliferativa e um aumento e/ou aceleração da diferenciação, como indicado por alterações na expressão gênica de marcadores do fenótipo osteoblástico. Portanto, essa modificação de superfície pode ter um impacto nos processos de reparo e remodelação do tecido ósseo adjacente a implantes, favorecendo a ocorrência de maior formação óssea.
Cellular and extracellular events that occur during titanium (Ti) osseointegration process are highly influenced by its surface properties, such as morphology, topography and chemical composition. The objective of biochemical modification of Ti is to immobilize proteins or peptides on its surface in order to induce specific cellular and tissue responses at the boneimplant interface in order to accelerate or enhance osseointegration. The aim of this study was to evaluate the osteoblastic phenotype development in cells grown on collagen type I-coated Ti surface. Osteoblastic cells from human alveolar bone fragments were cultured on turned Ti either coated with collagen type I (col-Ti) or not (turned-Ti) and the following parameters were assessed: cell adhesion, morphology, and proliferation, total protein content, alkaline phosphatase (ALP) activity, bone-like formation and gene expression of osteoblastic markers by real-time polymerase chain reaction (real-time PCR). Col-Ti altered culture growth and gene expression of osteoblastic markers without affecting cell adhesion, morphology, protein synthesis, ALP activity, and matrix mineralization. These results demonstrated that col-Ti favours cell growth during the proliferative phase and osteoblastic differentiation, as demonstrated by changes in mRNA expression profile during the matrix mineralization phase, suggesting that this Ti surface modification may affect the processes of bone healing and remodelling.
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Books on the topic "Alveolar type cell"

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Verfasser, Schließmann Stephan J., Kirschbaum Andreas Verfasser, Plönes Till 1976 Verfasser, Müller-Quernheim Joachim 1953 Verfasser, Zissel Gernot Verfasser, Klinik für Pneumologie, Albert-Ludwigs-Universität Freiburg Medizinische Fakultät, and Albert-Ludwigs-Universität Freiburg, eds. Roflumilast-N-oxide induces surfactant protein expression in human alveolar epithelial cells type II. Freiburg: Universität, 2012.

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Gandhi, Shephali G. The effect of pulmonary edema fluid on ion transport by adult alveolar type II epithelial cells. 2007.

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Book chapters on the topic "Alveolar type cell"

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Kauffman, Shirley L., and Tamiko Sato. "Alveolar Type II Cell Adenoma, Lung, Mouse." In Respiratory System, 102–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-96846-4_16.

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Panos, Ralph J. "Cytokines and Alveolar Type II Cells." In Cytokines of the Lung, 417–56. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003066927-17.

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Lwebuga-Mukasa, J. S. "Isolation of type Il alveolar epithelial cells." In Methods in Pulmonary Research, 387–401. Basel: Birkhäuser Basel, 1998. http://dx.doi.org/10.1007/978-3-0348-8855-4_15.

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Liu, Yuru. "Type II Cells as Progenitors in Alveolar Repair." In Lung Stem Cells in the Epithelium and Vasculature, 13–33. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-16232-4_2.

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Kosmider, Beata, Robert J. Mason, and Karim Bahmed. "Isolation and Characterization of Human Alveolar Type II Cells." In Methods in Molecular Biology, 83–90. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8570-8_7.

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Jansing, Nicole L., Jazalle McClendon, Hidenori Kage, Mitsuhiro Sunohara, Juan R. Alvarez, Zea Borok, and Rachel L. Zemans. "Isolation of Rat and Mouse Alveolar Type II Epithelial Cells." In Methods in Molecular Biology, 69–82. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8570-8_6.

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Burkhardt, R., P. von Wichert, J. J. Batenburg, and L. M. G. van Golde. "Regulation of Phosphatidylcholine Synthesis in Type II Alveolar Epithelial Cells." In Surfactant Replacement Therapy, 357–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73305-5_43.

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Thiedemann, K. U., I. Paulini, N. Lüthe, A. Kreft, U. Abel, U. Heinrich, U. Glaser, and U. Mohr. "Regeneration, Differentiation, and Neoplastic Transformation of Type II Alveolar Epithelial Cells." In Advances in Controlled Clinical Inhalation Studies, 185–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77176-7_18.

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Schließmann, Stephan J., K. Höhne, A. Charra, A. Kirschbaum, B. Cucuruz, S. Schumann, G. Zissel, and J. Guttmann. "Differences in form stability between human non-tumorous alveolar epithelial cells type 2 and alveolar carcinoma cells under biaxial stretching." In IFMBE Proceedings, 2027–30. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-89208-3_483.

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Gonzalez, Robert F., and Leland G. Dobbs. "Isolation and Culture of Alveolar Epithelial Type I and Type II Cells from Rat Lungs." In Methods in Molecular Biology, 145–59. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-125-7_10.

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Conference papers on the topic "Alveolar type cell"

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Li, C., N. Peinado, S. M. Smith, J. Zhou, F. Gao, G. Kohbodi, M. K. Lee, et al. "Wnt5a Promotes Alveolar Type 1 Cell Differentiation During Lung Development." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a5480.

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Driscoll, Barbara, Jooeun Lee, Raghava Reddy, Angelie Nguyen, Nandini Girish, Alexander Kikuchi, and Sha-Ron Jackson. "Distal Lung Regeneration Following Targeted Alveolar Epithelial Type 2 Cell Depletion." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4206.

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Zhang, D., L. A. Vickers, N. Gao, A. A. Sathe, C. Xing, and C. K. Garcia. "Single Cell Transcriptomic Profiling of Alveolar Epithelial Type 2 Cells in Sftpa1 G231V Mice." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a6144.

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Lehmann, M., Q. Hu, Y. Hu, M. Ansari, R. Pineda, W. J. Janssen, H. Schiller, F. Theiss, and M. Koenigshoff. "Inflammaging and Impaired Progenitor Cell Function in Aged Alveolar Epithelial Type (AT) II Cells." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4205.

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Kulish, Vladimir V., José L. Lage, Connie C. W. Hsia, and Robert L. Johnson. "Red Blood Cell Distribution Effect on Lung Diffusing Capacity: A Macroscopic Analysis." In ASME 2000 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/imece2000-2228.

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Abstract A novel mathematical model derived from fundamental engineering principles for simulating the spatial and temporal gas diffusion process within the alveolar region of the lung was presented recently by Koulich et al. [1]. The model depends on a physical property of the alveolar region termed effective diffusivity, function of the diffusivity, solubility, and interface geometry of each alveolar constituent. Unfortunately, the direct determination of the effective diffusivity of the alveolar region is impractical because of the difficulty in describing the internal geometry of each alveolar constituent. However, the transient solution of the macroscopic model can be used in conjunction with the lung diffusing capacity (measured in laboratory via the single-breath technique) to determine the effective diffusivity of the alveolar region. With the effective diffusivity known, the three-dimensional effects of red blood cell distribution on the lung diffusing capacity can be predicted via numerical simulations. The results, obtained for normal (random), uniform, center-cluster, corner-cluster, and several chain-like distributions, unveil a strong relationship between the type of cell distribution and the lung diffusing capacity.
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Korogi, Y., S. Gotoh, S. Ikeo, Y. Yamamoto, N. Sone, K. Tamai, S. Konishi, et al. "Alveolar Epithelial Type 2 Cell Dysfunction in Hermansky-Pudlak Syndrome Type 2 Patient-Derived Induced Pluripotent Stem Cells." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5268.

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Allawzi, A., R. Roy, N. Burns, W. J. Janssen, E. Nozik-Grayck, R. M. Tuder, and C. U. Vohwinkel. "Alveolar Type 2 Cell Dependent Lactate Resolves Alveolar Inflammation via Crosstalk with Resident Alveolar Macrophages in Two Models of Acute Lung Injury." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4500.

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Duong, T. E., B. Sos, LungMAP, J. S. Hagood, and K. Zhang. "Dynamic Single-Cell Chromatin Landscapes of Alveolar Type 1 Cell Populations in the Developing Lung." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4011.

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Balasubramaniam, V., EV Roth, G. Seedorf, S. Ryan, and SH Abman. "A Bone Marrow Myeloid Progenitor Cell Enhances Mouse Alveolar Type II Cell Growth In Vitro." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2406.

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Brandenberger, C., T. Yazicioglu, C. Autilio, C. Huang, C. Bär, T. Thum, J. Perez-Gil, A. Schmiedl, and C. Mühlfeld. "Aging causes alveolar epithelial type II cell dysfunction in acute lung injury." In ERS Lung Science Conference 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/23120541.lsc-2020.67.

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Reports on the topic "Alveolar type cell"

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Lin, Hongwei, Yanjun Gao, Kang Sun, and Faguang Jin. Association between PM2.5 pollution and outpatient visits for respiratory diseases in China: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0144.

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Review question / Objective: Previous epidemiological studies on the association between PM2.5 pollution and outpatient visits for respiratory diseases in China were mostly limited to one region， and the different papers have no coherent results. Our objective is to perform a systematic review and meta-analysis of the relevant literature in order to summarize the association between PM2.5 pollution and outpatient visits for respiratory diseases in multiple cities in China. Condition being studied: As an important component of air pollutants, particulate matter 2.5 (PM2.5) can float in the atmosphere for a long time with a small aerodynamic size (≤2.5μm) and large specific surface area which is attached to a variety of toxic and harmful substances . PM2.5 can deposite under the trachea of the respiratory tract, reaching deep into the alveolar area, damaging alveolar macrophages and type Ⅱ alveolar epithelial cells, inducing alveolar inflammation, resulting in decreased immunity of the respiratory tract and interfering with normal physiological functions of the lungs.
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