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Rozprawy doktorskie na temat „Lung alveolar cells”

Autor: Grafiati

Data publikacji: 3 czerwca 2025

Data aktualizacji: 31 lipca 2025

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1

Mattes, Charlott, and Ulrich H. Thome. "Rapid elevation of sodium transport through insulin is mediated by AKT in alveolar cells." Universitätsbibliothek Leipzig, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-142643.

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Alveolar fluid clearance is driven by vectorial Na+ transport and promotes postnatal lung adaptation. The effect of insulin on alveolar epithelial Na+ transport was studied in isolated alveolar cells from 18–19-day gestational age rat fetuses. Equivalent short-circuit currents (ISC) were measured in Ussing chambers and different kinase inhibitors were used to determine the pathway of insulin stimulation. In Western Blot measurements the activation of mediators stimulated by insulin was analyzed. The ISC showed a fast dose-dependent increase by insulin, which could be attributed to an increased

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2

Sitaraman, Sneha. "Alveolar type 2 epithelial cells in lung development and disease." University of Cincinnati / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1571062200291287.

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3

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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Cherlet, Tracy C. "Tetrahydrocannabinol and lung surfactant metabolism in isolated fetal type II alveolar cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0025/MQ51693.pdf.

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Barth, Kathrin, Robert Bläsche та Michael Kasper. "T1α/Podoplanin Shows Raft-Associated Distribution in Mouse Lung Alveolar Epithelial E10 Cells". Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-137577.

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Aims: T1α/(podoplanin) is abundantly expressed in the alveolar epithelial type I cells (ATI) of rodent and human lungs. Caveolin-1 is a classical primary structural protein of plasmalemal invaginations, so-called caveolae, which represent specialized lipid rafts, and which are particularly abundant in ATI cells. The biological functions of T1α in the alveolar epithelium are unknown. Here we report on the characteristics of raft domains in the microplicae/microvillar protrusions of ATI cells, which contain T1α. Methods: Detergent resistant membranes (DRMs) from cell lysates of the mouse epithel

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Barth, Kathrin, Robert Bläsche та Michael Kasper. "T1α/Podoplanin Shows Raft-Associated Distribution in Mouse Lung Alveolar Epithelial E10 Cells". Karger, 2010. https://tud.qucosa.de/id/qucosa%3A27742.

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Aims: T1α/(podoplanin) is abundantly expressed in the alveolar epithelial type I cells (ATI) of rodent and human lungs. Caveolin-1 is a classical primary structural protein of plasmalemal invaginations, so-called caveolae, which represent specialized lipid rafts, and which are particularly abundant in ATI cells. The biological functions of T1α in the alveolar epithelium are unknown. Here we report on the characteristics of raft domains in the microplicae/microvillar protrusions of ATI cells, which contain T1α. Methods: Detergent resistant membranes (DRMs) from cell lysates of the mouse epithel

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7

Naranjo, Santiago(Santiago Jose). "An organoid platform to study alveolar stem cells in lung generation and cancer." Thesis, Massachusetts Institute of Technology, 2020. https://hdl.handle.net/1721.1/129032.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, 2020<br>Cataloged from student-submitted PDF of thesis. Vita.<br>Includes bibliographical references.<br>Lung adenocarcinoma (LADC) remains the most common and lethal cancer type worldwide. Although recent breakthroughs using a new class of immune-modulatory therapeutics have improved patient survival in the clinic, the majority still invariably succumb to this disease, highlighting the importance of improving treatment strategies. A wide variety of models have been developed to study LADC. Cell line- and transplant-

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8

Medina-Tato, David A. "Role of phosphoinositide 3-kinase in TNFα signalling in A549 lung alveolar cells". Thesis, University of Bath, 2007. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441522.

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9

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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10

Wong, Yin-ling. "The effects of respiratory syncytial virus on alveolar epithelial cells toll-like receptors expressions and T cell apoptosis." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B4218230X.

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11

Chuquimia, Flores Olga Daniela. "Role of alveolar epithelial cells in macrophage responses against mycobacterial infections." Doctoral thesis, Stockholms universitet, Institutionen för molekylär biovetenskap, Wenner-Grens institut, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-86776.

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This thesis aimed to investigate the role of alveolar epithelial cells (AEC) on immune responses against mycobacterial infections, specifically, the role of AEC in modulating macrophage functions through the secretion of broad variety of factors. In paper I, we compared murine AEC with interstitial macrophages (PuM) in their ability to take up and control mycobacterial growth and their capacity as antigen-presenting cells. We found that AEC were able to internalize and control bacterial growth and present antigens to T cells from immunized mice. In addition, both AEC and PuM exhibited distinct

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12

Eghtesad-Farahi, Marjan. "Investigation of the role of human alveolar epithelial cells in the traffic of immune cells into the lung." Thesis, University of Sunderland, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.420481.

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13

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

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14

Scordo, Julia Marianna. "Impact of the Human Lung Mucosa on Mycobacterium tuberculosis Infection of Alveolar Epithelial Cells." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1542718137103233.

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15

Wong, Yin-ling, and 王燕玲. "The effects of respiratory syncytial virus on alveolar epithelial cells toll-like receptors expressions and T cell apoptosis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B4218230X.

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16

Endicott, Roger A. "Immunoregulation of T-lymphocyte proliferative activity by alveolar macrophages from mice bearing Lewis lung carcinoma tumors." Virtual Press, 1986. http://liblink.bsu.edu/uhtbin/catkey/458971.

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The immune regulatory abilities of alveolar macrophages from C57B1/6 mice bearing a metastatic variant of Lewis lung carcinoma were determined. During early stages of tumor development, or before tumors metastasized to the lungs, alveolar macrophages did not affect or slightly enhanced T-lymphocyte proliferation; as tumor growth progressed, or following tumor metastasis, alveolar macrophages suppressed the T-cell response. Macrophage suppressor activity was probably not mediated by their production of PGE, since macrophages of tumor-bearing mice secreted less 2 PGE than did macrophages of norm

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17

Perry, Mark Michael. "The role of microRNA-146a in the IL-1B-induced inflammatory response in human lung alveolar epithelial cells." Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.505001.

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18

Garrison, Derek S. "Rationale for the Study of Fatty Acid Binding Protein 5 in Alveolar Type II Cells." University of Cincinnati / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1226862267.

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19

Chahwan, Valéria. "Sirpα-SHP2 signalling pathway in alveolar macrophages during bacterial pneumonia". Electronic Thesis or Diss., Nantes Université, 2025. http://www.theses.fr/2025NANU1044.

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Le sepsis augmente la susceptibilité à la pneumonie nosocomiale, en diminuant notamment la capacité phagocytaire des macrophages alvéolaires (AM). Après un premier épisode de pneumonie, les macrophages alvéolaires résidents (resAM) subissent une pression tolérogène, qui altère leur fonction phagocytaire. Cette adaptation n'est pas due à une exposition directe à l’agent pathogène, mais à des signaux immunosuppresseurs secondaires générés dans l'environnement. Nous avons montré que le récepteur Sirpα, principalement exprimé par les cellules myéloïdes, joue un rôle central dans la régulation de l

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20

Weinhold, Karina. "Molekulare und biochemische Charakterisierung der purinergen Rezeptoren P2X4 und P2X7 im Alveolarepithel der Lunge." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2010. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-62141.

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Gegenstand der vorliegenden Arbeit sind die purinergen Rezeptoren P2X4R und P2X7R. Die P2XR werden durch ATP aktiviert und stellen unselektive Kationenkanäle dar, die auch für Ca2+ durchlässig sind. Beiden P2XR-Subtypen werden in den Alveolarepithel Typ I (AT I)-Zellen der Lunge exprimiert und aufgrund ihrer Kanalaktivitäten in Zusammenhang mit der alveolären Flüssigkeitshomöostase gebracht. Bei bisherigen Untersuchungen wurde jedoch die mögliche Assoziation und Modulation der P2XR durch Mikrodomänen der Zellmembran außer Acht gelassen. Ein Modell von Garcia-Marcos zeigt, dass P2X7R in Zellen

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21

Samuels, Emile Rasheed. "Calcium²§+-PS-dependent protein kinase C activity in fetal, neonate and adult rabbit lung and the release of surfactant-related material from isolated fetal rabbit type II alveolar cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq23487.pdf.

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22

Marten, Elger [Verfasser], and Christiane [Akademischer Betreuer] Dammann. "Interdependent TTF1 - ErbB4 interactions are critical for surfactant protein-B homeostasis in primary mouse lung alveolar type II cells / Elger Marten ; Akademischer Betreuer: Christiane Dammann ; Zentrum Kinderheilkunde und Jugendmedizin Abteilung Pädiatrische Pneumologie und Neonatologie der Medizinischen Hochschule Hannover." Hannover : Bibliothek der Medizinischen Hochschule Hannover, 2016. http://d-nb.info/1108556582/34.

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23

Hosker, Harold Stephen Ronald. "Alveolar macrophage and blood monocyte function in small cell lung cancer." Thesis, University of Newcastle Upon Tyne, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.241364.

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24

Lauzon, Wallace Delbert. "The functional characterization of lung-associated natural killer activity and its regulation by alveolar macrophages." Thesis, University of Ottawa (Canada), 1995. http://hdl.handle.net/10393/9919.

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The purpose of this study was to characterize the natural killer activity of lymphocytes resident in the rat lung and explore its modulation. Lung lymphocytes (LL) were shown to possess potent NK activity against Yac-1 targets, The effector cells were found to be sensitive to complement-mediated lysis with anti-asialo GM-1 and to treatment with L-leucine methyl ester, which selectively kill NK cells. LL were more potent NK effectors than peripheral blood (PBL) or spleen lymphocytes (SL), although the lung and spleen contained similar proportions of NK (3.2.3 positive) cells. Lung and periphera

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25

Kanj, Rania S. "Interaction between primary alveolar macrophages and primary alveolar type II cells under basal conditions and after lipopolysaccharide or quartz exposure." Morgantown, W. Va. : [West Virginia University Libraries], 2004. https://etd.wvu.edu/etd/controller.jsp?moduleName=documentdata&jsp%5FetdId=34.

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Thesis (Ph. D.)--West Virginia University, 2004.<br>Title from document title page. Document formatted into pages; contains x, 130 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 120-130).

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26

VOLPE, MARIA CONCETTA. "miR-200c prevents and reverts Lung fibrosis by down regulating Flt1 and promoting lung regeneration." Doctoral thesis, Università degli Studi di Trieste, 2022. http://hdl.handle.net/11368/3014982.

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Idiopathic pulmonary fibrosis (IPF) is a devastating progressive fibrotic disease affecting the lungs and causing chronic respiratory failure. In IPF, adult alveolar type II stem cells (ATII) cannot trans-differentiate to alveolar type I cells (ATI), and therefore, represents a relevant target in the progression of lung fibrosis. There are only two FDA-approved drugs for the treatment of IPF, which can only ameliorate the disease, but a permanent cure is not yet available. In this work, we showed that human ATII cells isolated from IPF patients displayed impaired trans-differentiation in vitro

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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. aure

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Robinson, Adam Benjamin. "The Pro-Inflammatory Contributions of Receptors for Advanced Glycation End-Products (RAGE) in Alveolar Macrophages Following Cigarette Smoke Exposure." BYU ScholarsArchive, 2012. https://scholarsarchive.byu.edu/etd/3253.

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Receptors for advanced glycation end-products (RAGE) are multi-ligand cell surface receptors of the immunoglobin family expressed by epithelium and macrophages. RAGE expression increases following ligand binding and when diverse cells are exposed to a variety of insults including cigarette smoke extract (CSE). The current research sought to characterize the pro-inflammatory contributions of RAGE expressed by alveolar macrophages (AMs) following CSE exposure. Acute exposure of mice to CSE via nasal instillation revealed diminished bronchoalveolar lavage (BAL) cellularity and fewer AMs in RAGE n

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Young, Bethany M. "ENGINEERING THE ALVEOLAR GAS EXCHANGE BARRIER WITH EXTRACELLULAR MATRIX COATINGS FOR BIOENGINEERED LUNGS." VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/5973.

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Lower respiratory diseases are currently the third leading cause of death worldwide. For many end-stage patients with these diseases, there is no cure and a shortage of donor organs available for transplant. A promising solution is to design regenerative scaffolds or complete bioengineered lungs, using decellularized lung tissues as a template for regeneration. Recent advances in the field have made significant strides towards developing a transplantable lung. However, the current technology has not produced a functional lung for in vivo transplant due to immature gas exchange barriers. The me

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Eerola, A. K. (Anna-Kaisa). "Apoptosis and apoptosis regulating proteins and factors in small and large cell lung carcinoma." Doctoral thesis, University of Oulu, 1999. http://urn.fi/urn:isbn:9514254066.

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Abstract Aptosis denotes a biochemically and morphologically distinct chain of events leading to self-destruction of cell. It is pivotal in the maintenance of tissue homeostasis and also plays a role in neoplasm. In this work, the extent of apoptosis and apoptosis regulating proteins and factors was studied in a total of 94 patients operated for lung carcinoma, including 56 small cell lung carcinomas (SCLC) and 38 large cell lung carcinomas (LCLC). The extent of apoptosis was determined by detecting and counting the relative and absolute numbers of apoptotic cells and bodies using 3'- end labe

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Redente, Elizabeth Frances. "Macrophage and bone marrow derived monocyte activation during mouse lung tumorigenesis and chronic inflammation /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2008.

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Thesis (Ph.D. in Toxicology) -- University of Colorado Denver, 2008.<br>Typescript. Includes bibliographical references (leaves 224-253). Free to UCD Anschutz Medical Campus. Online version available via ProQuest Digital Dissertations;

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32

Peters, Dorothea Maren [Verfasser]. "TGF-beta mediates alveolar fluid balance by regulating the cell-surface stability of the epithelial sodium channel in the lung / Dorothea Maren Peters." Gießen : Universitätsbibliothek, 2011. http://d-nb.info/1063110807/34.

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Chang, Christopher J. "Using MicroRNAs 146a and 155 to Mitigate Barotrauma and Atelectrauma in Simulated Ventilator-Induced Lung Injury." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1524188199388787.

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Moliva, Juan Ignacio. "The Lung Mucosa and its Impact on Mycobacterium tuberculosis Pathogenesis and Bacillus Calmette-Guerin Vaccine Efficacy." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1497602977755499.

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Jabaudon, Gandet Matthieu. "Approche translationnelle de la voie RAGE au cours du syndrôme de détresse respiratoire aiguë : implications diagnostiques, physiopathologiques et thérapeutiques." Thesis, Clermont-Ferrand 1, 2016. http://www.theses.fr/2016CLF1MM09.

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Le syndrome de détresse respiratoire aiguë (SDRA) est caractérisé par des lésions alvéolaires diffuses menant à un œdème alvéolaire lésionnel et une insuffisance respiratoire aiguë hypoxémique. Malgré les progrès récents dans la prise en charge des patients de réanimation, le SDRA reste un syndrome fréquent et associé à une morbimortalité importante. Deux mécanismes principaux du SDRA semblent associés à une mortalité plus élevée et à des réponses thérapeutiques différentes : la déficience de la clairance liquidienne alvéolaire (AFC, pour alveolar fluid clearance), l’incapacité pour l’épithéli

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Jacob, Anjali. "Generation of mature type II alveolar epithelial cells from human pluripotent stem cells." Thesis, 2017. https://hdl.handle.net/2144/26476.

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Tissues arising late in evolutionary time, such as lung alveoli that are unique to air breathing organisms, have been challenging to generate in vitro from pluripotent stem cells (PSCs), in part because there are limited lower organism model systems available to provide the necessary developmental roadmaps to guide in vitro differentiation. Furthermore, pulmonary alveolar epithelial type II cell (AEC2) dysfunction has been implicated as a primary cause of pathogenesis in many poorly understood lung diseases that lack effective therapies, including interstitial lung disease (ILD) and emphysema.

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Merluza, John. "Nicotine and cotinine effects on fetal rat lung type II alveolar cells." 2006. http://hdl.handle.net/1993/20898.

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Sun, Yuliang Leon. "The role of ATP binding cassette A3 (ABCA3) in health and disease using pluripotent stem cell-derived type II alveolar epithelial cells." Thesis, 2020. https://hdl.handle.net/2144/41103.

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The most common causes of childhood interstitial lung disease (chILD) are autosomal recessive mutations in the gene encoding ATP Binding Cassette A3 (ABCA3) protein, a lamellar body (LB) associated lipid transporter exclusively expressed within the alveolar epithelial type II cells (AEC2s) in the lung. Instability of primary AEC2s in culture has prevented studies of ABCA3 mutations, resulting in limited understanding of disease pathogenesis. To overcome this challenge, we developed AEC2-like cells from human pluripotent stem cells (PSCs) in vitro, allowing study of normal ABCA3 function and pe

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Ahmed, Asra. "Apoptosis and caspase-3 activity in isolated fetal rat lung cells, human A549 cells and rat periodontal ligament fibroblasts following exposure to cigarette smoke extract." 2012. http://hdl.handle.net/1993/5205.

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Exposure cigarette smoke (CS) during prenatal life is the leading cause of preventable premature death. In this study, we explored the hypothesis that in vitro exposure of fetal lung cells to cigarette smoke extract (CSE) may result in the alteration of apoptosis through activation of caspase-3. Alongside we compared the responses of fetal lung cells with A549 cells and rat periodontal ligament (PDL) fibroblasts exposed to CSE in a dose dependent manner. Caspase-3 activity and inhibition was measured using a fluorometric assay. Cell viability in smoke exposed cells was measured using MTT forma

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Lee, Chou-hwei, and 李秋慧. "Autologous Transplantation of Endothelial Progenitor Cells Improves Pulmonary Gas Exchange and Reduces Alveolar Inflammation in Rabbits with Acute Lung Injury." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/19750122642258342442.

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碩士<br>國立成功大學<br>細胞生物及解剖學研究所<br>97<br>Acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS) are the most common causes of death in intensive care units and after major operation. The fundamental pathogenesis of ALI is increased alveolocapillary permeability largely due to inflammatory response in the pulmonary endothelium and alveoli. Activation and damage of pulmonary endothelium is another hallmark of ALI/ARDS. A number of endothelium-targeting therapies have been tested in clinical settings, but none of these restores pulmonary endothelial function during ALI/ARDS. Accum

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Litvack, Michael L. "Effect of Innate Immune Collectin Surfactant Protein D and Adaptive Immune Protein IgM on Enhancing Clearance of Late Apoptotic Cells by Alveolar Macrophages." Thesis, 2011. http://hdl.handle.net/1807/29793.

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The innate immune protein surfactant protein (SP-) D is a carbohydrate binding protein that was originally isolated from mucosal lung tissues. Recently, studies show that SP-D binds to antibodies, including immunoglobulin M (IgM), which interacts with late apoptotic cells. Here we focus on the interaction between SP-D and IgM as they pertain to late apoptotic cell clearance. We hypothesized that the three-way interaction between IgM, SP-D and late apoptotic cells is functionally applicable to clearing late apoptotic cells from the lungs, thereby reducing lung inflammation. We show that SP-D bi

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42

Chuang, Chi-Yuan, and 莊淇源. "STUDY OF ACUTE LUNG INJURY: MOLECULAR MECHANISMS OF LIPOPOLYSACCHARIDE-INDUCED APOPTOTIC INSULTS AND REGULATION OF surfactant protein GENE EXPRESSION IN HUMAN ALVEOLAR EPITHELIAL TYPE II CELLS." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/03097245032120426995.

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博士<br>臺北醫學大學<br>臨床醫學研究所<br>99<br>Lipopolysaccharide (LPS), a Gram-negative bacterial outer membrane component, is one of the major causes of septic shock with acute lung injury. Pulmonary alveolar epithelial type II cells have highly specialized functions for synthesizing and secreting surfactant proteins (SPs) to participate in the physiological and pathophysiological regulation of sepsis-induced acute lung injury. Alterations in the levels of surfactant components in the lungs during inflammation are quite complex. Toll-like receptors (TLRs) that play important roles in innate immunity can t

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Samuels, Emile Rasheed. "Calcium2S+-PS-dependent protein kinase C activity in fetal, neonate and adult rabbit lung and the release of surfactant-related material from isolated fetal rabbit type II alveolar cells." 1996. http://hdl.handle.net/1993/1025.

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The fetal lung secretes significant quantities of surfactant during late gestation in preparation for respiration which must begin immediately after birth. Although initiation of surfactant synthesis/secretion may be accelerated, the underlying mechanisms of the process itself remain to be resolved. An important pathway in adult lung has implicated the a$\sp{2+}$-PS-dependent enzyme protein kinase C (PKC) in its regulation. The present study was undertaken to characterize the activity of Ca$\sp{2+}$-PS-dependent PKC in adult lung and to determine if PKC was involved in the processes of initiat

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Kaiser, Katherine. "Amphiregulin-producing regulatory T cells guide alveolar regeneration during influenza infection." Thesis, 2021. https://doi.org/10.7916/d8-phn6-7g45.

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The hematopoietic system has long been charactered for its essential function in protecting against pathogens, but it is increasingly established that immune cells play integral roles in resolving inflammation and driving tissue repair. While many cell types are recruited to the site of injury and participate in coordinated immune responses, regulatory T (Treg) cells have emerged as key players of tissue protection by limiting damage and promoting regeneration in multiple organ systems. A conserved feature of “pro-repair” Treg cells is their expression of amphiregulin (Areg), an epidermal grow

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Tan, Ju Jing. "Mechanosensitive ATP release in the lungs." Thesis, 2019. http://hdl.handle.net/1866/24849.

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L’ATP est bien connue pour son rôle de transporteur d'énergie à l’intérieur des cellules, mais en dehors de la cellule, elle agit en tant que molécule de signalisation extracellulaire. En se liant aux récepteurs purinergiques, l’ATP extracellulaire amorce la signalisation purinergique afin de réguler certains processus physiologiques et pathophysiologiques. Dans les poumons, l’ATP stimule la sécrétion de surfactant et promeut la clairance mucociliaire. Compte tenu du rôle critique de l’ATP extracellulaire dans les poumons, il est important de comprendre le mécanisme du relargage d’ATP cellulai

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Lo, Bernice. "Regulation of Adaptive Immunity in the Lung by the Alveolar Epithelial Type II Cell and Surfactant Protein a." Diss., 2008. http://hdl.handle.net/10161/711.

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<p>Due to its nature and function, the lungs are confronted with the unique challenge of rapidly eliminating inhaled pathogens and particulates while limiting inflammatory responses. A disruption in this immune homeostasis may result in respiratory inflammatory diseases, such as allergies or asthma. The alveolar epithelial type II cell and its secretory product, surfactant protein A (SP-A), have been linked to roles in adaptive immunity in the lung. The discovery that type II cells constitutively express major histocompatibility complex class II (MHC II) suggested that type II cells may fun

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Kamocki, Krzysztof. "The role of ceramides in cigarette smoke-induced alveolar cell death." Thesis, 2013. http://hdl.handle.net/1805/3311.

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Indiana University-Purdue University Indianapolis (IUPUI)<br>The complex pathogenesis of emphysema involves disappearance of alveolar structures, in part attributed to alveolar cell apoptosis. The mechanism by which cigarette smoke (CS) induces alveolar cell apoptosis is not known. We hypothesized that ceramides are induced by CS via specific enzymatic pathways that can be manipulated to reduce lung cell apoptosis. CS increased ceramides in the whole lung and in cultured primary structural lung cells. Exposure to CS activated within minutes the acid sphingomyelinase, and within weeks the de no

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Ramos, Sara Vilabril. "Microengineered 3D in vitro model of human pulmonary alveoli: Curvature's influence on lung epithelial cells." Master's thesis, 2017. http://hdl.handle.net/10316/83338.

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Trabalho de Projeto do Mestrado Integrado em Engenharia Biomédica apresentado à Faculdade de Ciências e Tecnologia<br>A engenharia de tecidos visa criar modelos in vitro de tecidos e estruturas biológicas funcionais recorrendo a diferentes tecnologias, conforme o objectivo final. Uma estratégia importante para adquirir um bom conhecimento do funcionamento dos órgãos humanos e da sua interações enquanto sistema biológico passa por devenvolver modelos in vitro que representem, da melhor forma possível, a sua anatomia e fisiologia.Desenvolvimento de um modelo 3D in vitro de alvéolo humano por mic

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Mothibeli, Keitumetse. "The effect of maternal nicotine exposure on cell proliferation on the lungs of the offspring." 2013. http://hdl.handle.net/11394/3753.

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>Magister Scientiae - MSc<br>Tobacco consumption and exposure to tobacco smoke is one of the biggest contributing factors to a growing epidemic of non-communicable diseases (NCDs), primarily cancers, diabetes, cardiovascular and chronic lung diseases which account for 63% of all deaths worldwide (WHO, 2011). An increased concern is in pregnant women who smoke. They not only expose themselves to nicotine, but also their unborn child. Cigarette smoking during pregnancy is associated with many developmental and growth complications. There are critical periods within the “program” that directs nor

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