Mechanisms of liquid flux across pulmonary alveolar epithelial cell monolayers

Filippatos, Gerasimos; Hughes, William F.; Qiao, Renli; Sznajder, Jacob I.; Uhal, Bruce D.

doi:10.1007/s11626-997-0141-z

Cited by 19 publications

(8 citation statements)

References 40 publications

(46 reference statements)

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“…Previously, it was thought that the AT2 cell is responsible for the majority of the vectorial transport of Na ϩ across the alveolar epithelial barrier (56,68,109,110,114,123,154). However, recently, an important role for AT1 cell in vectorial Na ϩ transport has been demonstrated, and it appears that the ␣ 2 Na-K-ATPase isozyme expressed mostly in AT1 cells is responsible for ϳ60% of Na ϩ transport (23, 89,154,155).…”

Section: Alveolar Epitheliummentioning

confidence: 99%

Mechanisms of pulmonary edema clearance

Mutlu

Sznajder

2005

American Journal of Physiology-Lung Cellular and Molecular Phys

165

140

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The mechanisms of pulmonary edema resolution are different from those regulating edema formation. Absorption of excess alveolar fluid is an active process that involves vectorial transport of Na+ out of alveolar air spaces with water following the Na+ osmotic gradient. Active Na+ transport across the alveolar epithelium is regulated via apical Na+ and chloride channels and basolateral Na-K-ATPase in normal and injured lungs. During lung injury, mechanisms regulating alveolar fluid reabsorption are inhibited by yet unclear pathways and can be upregulated by pharmacological means. Better understanding of the mechanisms that regulate edema clearance may lead to therapeutic interventions to improve the ability of lungs to clear fluid, which is of clinical significance.

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Section: Alveolar Epitheliummentioning

confidence: 99%

Mechanisms of pulmonary edema clearance

Mutlu

Sznajder

2005

American Journal of Physiology-Lung Cellular and Molecular Phys

165

140

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“…The morphologic and functional status of the monolayers on the filters was assessed by fluorescence microscopy as previously described by Filippatos et al [11]. The adherent monolayers were fixed with 70% ethanol at 4°C for 30 min.…”

Section: Light Microscopymentioning

confidence: 99%

Protection of Meconium-Induced Lung Epithelial Injury by Protease Inhibitors

Ota

Gopallawa

Ivanov

et al. 2017

JLPRR

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Earlier work form this laboratory showed that exposure of alveolar epithelial cells (AECs) to meconium caused significant cell detachment and that meconium-induced detachment of cells was prevented by a protease inhibitor cocktail. Therefore, it was hypothesized that protease inhibitors might protect AEC monolayers against meconium-induced collapse of epithelial barrier function both in vitro and in vivo. To investigate this theory in vitro, albumin flux was measured across cultured, confluent monolayers of human type II derived cell line A549 on microporous filter inserts. Human meconium was collected from seven healthy full-term neonates and the samples were pooled and diluted prior to analysis. Exposure of AECs to 5% human meconium increased albumin flux across the cultured AEC monolayers, but the increase was significantly blocked by protease inhibitors (P<0.001). In C57/BL6 mice, intratracheal instillation of 5% human meconium increased the passage of Evans Blue Dye (EBD) from the vascular compartment into the alveolar spaces, measured in bronchoalveolar lavage (BAL) fluid after intravenous injection of EBD. Moreover, intratrachial coinstillation of protease inhibitors prevented the meconium-induced increase in EBD passage into BAL fluid (P<0.01). The data presented herein clearly demonstrate that protease inhibitors protect AEC barrier function against meconiuminduced injury, and suggest the future possibility of using protease inhibitors in the treatment of meconium aspiration syndrome.

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“…Further, the physiologic ability of alveolar epithelial cells to clear alveolar spaces from excess fluid is an active signalling process involving ion channels, mechanosensitive receptors, or adrenoreceptors. 19,20,21,25 Very recent data suggest that targeting mechanisms that prevent barrier dysfunction 26 and augment transepithelial sodium transport and enhance the clearance of alveolar oedema may lead to more effective prevention or treatment for PO. 25,33 A search for the precipitant and underlying aetiology must be conducted early in the course of hospitalisation.…”

Section: An Increase Of Left Ventricular (Lv) Filling Pressure and Immentioning

confidence: 99%

Pulmonary Oedema—Therapeutic Targets

Chioncel

Collins

Ambrosy

et al. 2015

Cardiac Failure Review

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Pulmonary oedema (PO) is a common manifestation of acute heart failure (AHF) and is associated with a high-acuity presentation and with poor in-hospital outcomes. The clinical picture of PO is dominated by signs of pulmonary congestion, and its pathogenesis has been attributed predominantly to an imbalance in Starling forces across the alveolarcapillary barrier. However, recent studies have demonstrated that PO formation and resolution is critically regulated by active endothelial and alveolar signalling. PO represents a medical emergency and treatment should be individually tailored to the urgency of the presentation and acute haemodynamic characteristics. Although, the majority of patients admitted with PO rapidly improve as result of conventional intravenous (IV) therapies, treatment of PO remains largely opinion based as there is a general lack of good evidence to guide therapy. Furthermore, none of these therapies showed simultaneous benefit for symptomatic relief, haemodynamic improvement, increased survival and end-organ protection. Future research is required to develop innovative pharmacotherapies capable of relieving congestion while simultaneously preventing end-organ damage.

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Mechanisms of liquid flux across pulmonary alveolar epithelial cell monolayers

Cited by 19 publications

References 40 publications

Mechanisms of pulmonary edema clearance

Mechanisms of pulmonary edema clearance

Protection of Meconium-Induced Lung Epithelial Injury by Protease Inhibitors

Pulmonary Oedema—Therapeutic Targets

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