scholarly journals Alveolar Type II Cells or Mesenchymal Stem Cells: Comparison of Two Different Cell Therapies for the Treatment of Acute Lung Injury in Rats

Cells ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 1816
Author(s):  
Raquel Guillamat-Prats ◽  
Marta Camprubí-Rimblas ◽  
Ferranda Puig ◽  
Raquel Herrero ◽  
Neus Tantinyà ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Molecular Mechanisms ◽  
Lung Damage ◽  
Alveolar Type ◽  
Therapeutic Effects ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Cell Therapies

The use of cell therapies has recently increased for the treatment of pulmonary diseases. Mesenchymal stem/stromal cells (MSCs) and alveolar type II cells (ATII) are the main cell-based therapies used for the treatment of acute respiratory distress syndrome (ARDS). Many pre-clinical studies have shown that both therapies generate positive outcomes; however, the differences in the efficiency of MSCs or ATII for reducing lung damage remains to be studied. We compared the potential of both cell therapies, administering them using the same route and dose and equal time points in a sustained acute lung injury (ALI) model. We found that the MSCs and ATII cells have similar therapeutic effects when we tested them in a hydrochloric acid and lipopolysaccharide (HCl-LPS) two-hit ALI model. Both therapies were able to reduce proinflammatory cytokines, decrease neutrophil infiltration, reduce permeability, and moderate hemorrhage and interstitial edema. Although MSCs and ATII cells have been described as targeting different cellular and molecular mechanisms, our data indicates that both cell therapies are successful for the treatment of ALI, with similar beneficial results. Understanding direct cell crosstalk and the factors released from each cell will open the door to more accurate drugs being able to target specific pathways and offer new curative options for ARDS.

Cell therapy for the treatment of acute lung injury: Alveolar type II cells or mesenchymal stem cells?

2016 ◽  
Author(s):  
Raquel Guillamat-Prats ◽  
Marta Camprubí-Rimblas ◽  
Ferranda Puig ◽  
Raquel Herrero ◽  
Anna Serrano-Mollar ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Cell Therapy ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells

scholarly journals Effect of the alveolar type ii cells transplantation for the treatment of acute lung injury

2015 ◽  
Vol 3 (S1) ◽  
Author(s):  
R Guillamat-Prats ◽  
F Puig ◽  
R Herrero ◽  
A Serrano-Mollar ◽  
M Camprubí-Rimblas ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells

Intratracheal instillation of alveolar type II cells enhances recovery from acute lung injury in rats

2018 ◽  
Vol 37 (6) ◽  
pp. 782-791 ◽  
Author(s):  
Raquel Guillamat-Prats ◽  
Ferranda Puig ◽  
Marta Camprubí-Rimblas ◽  
Raquel Herrero ◽  
Anna Serrano-Mollar ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Intratracheal Instillation ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells

Effect of alveolar type II cells in acute lung injury model

2015 ◽  
Author(s):  
Raquel Guillamat-Prats ◽  
Ferranda Puig ◽  
Raquel Herrero ◽  
Anna Serrano-Mollar ◽  
Marta Camprubí-Rimblas ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Injury Model ◽  
Lung Injury Model

Wound-induced calcium waves in alveolar type II cells

1997 ◽  
Vol 273 (6) ◽  
pp. L1242-L1248 ◽  
Author(s):  
Lee E. Hinman ◽  
Greg J. Beilman ◽  
Kristine E. Groehler ◽  
Paul J. Sammak
Keyword(s):  
Acute Lung Injury ◽  
Cyclopiazonic Acid ◽  
Alveolar Type ◽  
Calcium Waves ◽  
Type Ii Cells ◽  
Type Ii ◽  
Tetraacetic Acid ◽  
Alveolar Type Ii Cells ◽  
Soluble Factors ◽  
Intracellular Ca

Alveolar type II epithelial (ATII) cells repopulate the alveolus after acute lung injury. We hypothesized that injury would initiate signals in nearby survivors. When rat ATII monolayers were wounded, elevations in intracellular free Ca2+ concentration ([Ca2+]i) began at the edge of the wound and propagated outward as a wave for at least 300 μm. The [Ca2+]iwave was due to both influx of extracellular Ca2+ and release of intracellular Ca2+ stores. Reducing Ca2+ influx with brief treatments of ethylene glycol-bis(β-aminoethyl ether)- N, N, N′, N′-tetraacetic acid or Gd3+ reduced both the amplitude and the apparent speed. Draining intracellular Ca2+ stores by pretreatment with cyclopiazonic acid eliminated the [Ca2+]iwave. Therefore, the [Ca2+]iwave depended critically on intracellular Ca2+ stores. [Ca2+]ielevations propagated over a break in the monolayer, suggesting that extracellular pathways were involved. Furthermore, extracellular factors from injured cells elevated [Ca2+]iin uninjured cultures. We conclude that wounding produces a [Ca2+]iwave in surviving cells and part of this response is mediated by soluble factors released into the extracellular space during injury.

Elevation of KL-6, a lung epithelial cell marker, in plasma and epithelial lining fluid in acute respiratory distress syndrome

2004 ◽  
Vol 286 (6) ◽  
pp. L1088-L1094 ◽  
Author(s):  
Akitoshi Ishizaka ◽  
Tomoyuki Matsuda ◽  
Kurt H. Albertine ◽  
Hidefumi Koh ◽  
Sadatomo Tasaka ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Lung Injury ◽  
Distress Syndrome ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Epithelial Lining ◽  
Alveolar Type Ii Cells ◽  
Epithelial Lining Fluid ◽  
Lung Epithelial

KL-6 is a pulmonary epithelial mucin more prominently expressed on the surface membrane of alveolar type II cells when these cells are proliferating, stimulated, and/or injured. We hypothesized that high levels of KL-6 in epithelial lining fluid and plasma would reflect the severity of lung injury in patients with acute lung injury (ALI). Epithelial lining fluid was obtained at onset ( day 0) and day 1 of acute respiratory distress syndrome (ARDS)/ALI by bronchoscopic microsampling procedure in 35 patients. On day 0, KL-6 and albumin concentrations in epithelial lining fluid were significantly higher than in normal controls ( P < 0.001), and the concentrations of KL-6 in epithelial lining fluid ( P < 0.002) and in plasma ( P < 0.0001) were higher in nonsurvivors than in survivors of ALI/ARDS. These observations were corroborated by the immunohistochemical localization of KL-6 protein expression in the lungs of nonsurvivors with ALI and KL-6 secretion from cultured human alveolar type II cells stimulated by proinflammatory cytokines. Because injury to distal lung epithelial cells, including alveolar type II cells, is important in the pathogenesis of ALI, the elevation of KL-6 concentrations in plasma and epithelial lining fluid could be valuable indicators for poor prognosis in clinical ALI.

INDUCIBLE NITRIC OXIDE SYNTHASE EXPRESSION AND NUCLEAR FACTOR-κB ACTIVATION IN ALVEOLAR TYPE II CELLS IN LUNG INJURY

2001 ◽  
Vol 27 (6) ◽  
pp. 485-504 ◽  
Author(s):  
Hirohisa Toga ◽  
Takeyasu Tobe ◽  
Yoshimichi Ueda ◽  
Guan-Hu Yang ◽  
Kazuhiro Osanai ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Lung Injury ◽  
Nuclear Factor Κb ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Nuclear Factor ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Regulation of surfactant secretion in alveolar type II cells

2007 ◽  
Vol 293 (2) ◽  
pp. L259-L271 ◽  
Author(s):  
Alexandra V. Andreeva ◽  
Mikhail A. Kutuzov ◽  
Tatyana A. Voyno-Yasenetskaya
Keyword(s):  
Molecular Mechanisms ◽  
Lung Surfactant ◽  
Apical Plasma Membrane ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Lamellar Bodies ◽  
Alveolar Type Ii Cells ◽  
Air Liquid Interface ◽  
Recycled Material

Molecular mechanisms of surfactant delivery to the air/liquid interface in the lung, which is crucial to lower the surface tension, have been studied for more than two decades. Lung surfactant is synthesized in the alveolar type II cells. Its delivery to the cell surface is preceded by surfactant component synthesis, packaging into specialized organelles termed lamellar bodies, delivery to the apical plasma membrane and fusion. Secreted surfactant undergoes reuptake, intracellular processing, and finally resecretion of recycled material. This review focuses on the mechanisms of delivery of surfactant components to and their secretion from lamellar bodies. Lamellar bodies–independent secretion is also considered. Signal transduction pathways involved in regulation of these processes are discussed as well as disorders associated with their malfunction.

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