Architecture and Cellular Composition of the Air–Blood Tissue Barrier

Pinkerton, Kent E.; Gehr, Peter; Castañeda, Alejandro R.; Crapo, James D.

doi:10.1016/b978-0-12-404577-4.00009-6

Cited by 24 publications

(23 citation statements)

References 35 publications

(29 reference statements)

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“…It is possible that the differences in native ECM content of various species are due, in part, to the whether the animals are quadruped or bipedal, as mode of ambulation impacts breathing mechanics (34). The observed species-dependent lung properties reported in this work corroborate findings in the literature, including differences in alveolar size and septal thickness (35-38); GAG, collagen, and elastin content (17, 39); matrix stiffness (40, 41), and alveolar cellular composition (42, 43). …”

Section: Discussionsupporting

confidence: 89%

Comparative biology of decellularized lung matrix: Implications of species mismatch in regenerative medicine

et al. 2016

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Lung engineering is a promising technology, relying on re-seeding of either human or xenographic decellularized matrices with patient-derived pulmonary cells. Little is known about the species-specificity of decellularization in various models of lung regeneration, or if species dependent cell-matrix interactions exist within these systems. Therefore decellularized scaffolds were produced from rat, pig, primate and human lungs, and assessed by measuring residual DNA, mechanical properties, and key matrix proteins (collagen, elastin, glycosaminoglycans). To study intrinsic matrix biologic cues, human endothelial cells were seeded onto acellular slices and analyzed for markers of cell health and inflammation. Despite similar levels of collagen after decellularization, human and primate lungs were stiffer, contained more elastin, and retained fewer glycosaminoglycans than pig or rat lung scaffolds. Human endothelial cells seeded onto human and primate lung tissue demonstrated less expression of vascular cell adhesion molecule and activation of nuclear factor-κB compared to those seeded onto rodent or porcine tissue. Adhesion of endothelial cells was markedly enhanced on human and primate tissues. Our work suggests that species-dependent biologic cues intrinsic to lung extracellular matrix could have profound effects on attempts at lung regeneration.

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Section: Discussionsupporting

confidence: 89%

Comparative biology of decellularized lung matrix: Implications of species mismatch in regenerative medicine

et al. 2016

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“…This falls within the range of doses in our in vivo murine studies of 4 to 147 ng/cm 2 . This dosimetry calculation uses the literature approximation of 680 cm 2 for the surface area of the mouse epithelium (Pinkerton et al, 1992) and 1.12 cm 2 for the surface area of epithelial cells grown to confluence on the transwells. In our in vivo sub-acute inhalation study (Kim et al, 2011), mice were exposed 4 hr/day for 10 days and we delivered an estimated CuONP dose of 32 μg/mouse (47 ng/cm 2 ) which induced LDH release, very high chemokine production and cytotoxicity.…”

Section: Discussionmentioning

confidence: 99%

Toxicity of copper oxide nanoparticles in lung epithelial cells exposed at the air–liquid interface compared with in vivo assessment

Jing

Park

Peters

et al. 2015

Toxicology in Vitro

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The toxicity of spark-generated copper oxide nanoparticles (CuONPs) was evaluated in human bronchial epithelial cells (HBEC) and lung adenocarcinoma cells (A549 cells) using an in vitro air-liquid interface (ALI) exposure system. Dose-response results were compared to in vivo inhalation and instillation studies of CuONP. Cells were exposed to particle-free clean air (controls) or spark-generated CuONPs. The number median diameter, geometric standard deviation and total number concentration of CuONPs were 9.2 nm, 1.48 and 2.27×107 particles/cm3, respectively. Outcome measures included cell viability, cytotoxicity, oxidative stress and proinflammatory chemokine production. Exposure to clean air (2 or 4 hr) did not induce toxicity in HBEC or A549 cells. Compared with controls, CuONP exposures significantly reduced cell viability, increased lactate dehydrogenase (LDH) release and elevated levels of reactive oxygen species (ROS) and IL-8 in a dose-dependent manner. A549 cells were significantly more susceptible to CuONP effects than HBEC. Antioxidant treatment reduced CuONP-induced cytotoxicity. When dose was expressed per area of exposed epithelium there was good agreement of toxicity measures with murine in vivo studies. This demonstrates that in vitro ALI studies can provide meaningful data on nanotoxicity of metal oxides.

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“…Accumulation of 18 O in BALF cells and surfactant material suggests that 18 O 3 penetrates into the alveolar region of the lung during resting exposure. BALF cells and surfactant reside at the air-liquid interface and appear (from histological evidence) to have an alveolar origin 23. The fact that lung parenchyma following lavage contains very little 18 O following 18 O 3 exposure, as seen in a study involving rhesus monkeys,4 suggests that the reaction of 18 O 3 is concentrated at the air-liquid interface.…”

Section: Discussionmentioning

confidence: 99%

Biomarkers of Dose and Effect of Inhaled Ozone in Resting versus Exercising Human Subjects: Comparison with Resting Rats

et al. 2013

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To determine the influence of exercise on pulmonary dose of inhaled pollutants, we compared biomarkers of inhaled ozone (O3) dose and toxic effect between exercise levels in humans, and between humans and rats. Resting human subjects were exposed to labeled O3 (18O3, 0.4 ppm, for 2 hours) and alveolar O3 dose measured as the concentration of excess 18O in cells and extracellular material of nasal, bronchial, and bronchoalveolar lavage fluid (BALF). We related O3 dose to effects (changes in BALF protein, LDH, IL-6, and antioxidant substances) measurable in the BALF. A parallel study of resting subjects examined lung function (FEV1) changes following O3. Subjects exposed while resting had 18O concentrations in BALF cells that were 1/5th of those of exercising subjects and directly proportional to the amount of O3 breathed during exposure. Quantitative measures of alveolar O3 dose and toxicity that were observed previously in exercising subjects were greatly reduced or non-observable in O3 exposed resting subjects. Resting rats and resting humans were found to have a similar alveolar O3 dose.

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Architecture and Cellular Composition of the Air–Blood Tissue Barrier

Cited by 24 publications

References 35 publications

Comparative biology of decellularized lung matrix: Implications of species mismatch in regenerative medicine

Comparative biology of decellularized lung matrix: Implications of species mismatch in regenerative medicine

Toxicity of copper oxide nanoparticles in lung epithelial cells exposed at the air–liquid interface compared with in vivo assessment

Biomarkers of Dose and Effect of Inhaled Ozone in Resting versus Exercising Human Subjects: Comparison with Resting Rats

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