Rat lung alveolar type II cell line maintains sodium transport characteristics of primary culture

Michaut, Patrick; Planès, Carole; Escoubet, Brigitte; Clément, Annick; Clérici, Christine

doi:10.1002/(sici)1097-4652(199610)169:1<78::aid-jcp8>3.0.co;2-b

Cited by 14 publications

(9 citation statements)

References 30 publications

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“…Simian virus 40 (SV40)-transformed strain AT2 neonatal alveolar epithelial cells were used for the in vitro internalization assays (4). SV40-AT2 cells retain the sodium transport properties of alveolar type II cells and express RTI 40 (rat alveolar epithelial type I cell protein; molecular mass, approximately 40 kDa) (25,31). SV40-AT2 cells were grown in Dulbecco's modified Eagle's medium (DMEM) supplemented with 10% heat-inactivated fetal calf serum (FCS) (Labtech International, East Sussex, United Kingdom), penicillin (100 U/ml), and streptomycin sulfate (100 g/ml) (Invitrogen, Paisley, United Kingdom).…”

Section: Methodsmentioning

confidence: 99%

Increased Virulence of a Fibronectin-Binding Protein Mutant of Staphylococcus aureus in a Rat Model of Pneumonia

et al. 2002

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Fibronectin-binding proteins mediate Staphylococcus aureus internalization into nonphagocytic cells in vitro.We have investigated whether fibronectin-binding proteins are virulence factors in the pathogenesis of pneumonia by using S. aureus strain 8325-4 and isogenic mutants in which fibronectin-binding proteins were either deleted (DU5883) or overexpressed [DU5883(pFnBPA4)]. We first demonstrated that fibronectin-binding proteins mediate S. aureus internalization into alveolar epithelial cells in vitro and that S. aureus internalization into alveolar epithelial cells requires actin rearrangement and protein kinase activity. Second, we established a rat model of S. aureus-induced pneumonia and measured lung injury and bacterial survival at 24 and 96 h postinoculation. S. aureus growth and the extent of lung injury were both increased in rats inoculated with the deletion mutant (DU5883) in comparison with rats inoculated with the wild-type (8325-4) and the fibronectin-binding protein-overexpressing strain DU5883(pFnBPA4) at 24 h postinfection. Morphological evaluation of infected lungs at the light and electron microscopic levels demonstrated that S. aureus was present within neutrophils from both 8325-4-and DU5883-inoculated lungs. Our data suggest that fibronectin-binding protein-mediated internalization into alveolar epithelial cells is not a virulence mechanism in a rat model of pneumonia. Instead, our data suggest that fibronectin-binding proteins decrease the virulence of S. aureus in pneumonia.In a recent survey, Staphylococcus aureus was found to be the most common cause of lower respiratory tract infections in Europe, the United States, Canada, Latin America, and the Western Pacific region (9). In view of the fact that S. aureus infections are increasingly difficult to treat because of the high percentage of antibiotic-resistant strains (34), a better understanding of the molecular basis of S. aureus virulence in pneumonia may help in the design of new therapeutic strategies.S. aureus has long been regarded as an extracellular pathogen because it is rarely observed inside cells in vivo and because it secretes a range of toxins that are cytolytic to many host cell types (14, 29). However, recent in vitro studies demonstrate that S. aureus is internalized and survives inside nonphagocytic cells (1,2,12,18,19,21). Fibronectin-binding proteins present on the surface of S. aureus (16,19,26) mediate internalization into nonphagocytic cells. S. aureus fibronectin-binding proteins bind ␤1-integrins on the surface of the host cells by means of a fibronectin bridge (16).Survival of internalized S. aureus within nonphagocytic cells may be an additional virulence mechanism in S. aureus infections (20). Internalized S. aureus may be able to evade or delay elimination by the host's immune system and avoid extracellular antibiotics (20). If internalization contributes to S. aureus persistence in vivo, then drugs which interfere with fibronectin binding to host cell integrins may have a role to play in treatment of S. a...

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Section: Methodsmentioning

confidence: 99%

Increased Virulence of a Fibronectin-Binding Protein Mutant of Staphylococcus aureus in a Rat Model of Pneumonia

et al. 2002

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“…The alveolar type II cell is responsible for the secretion of surfactant (65, 66) as well as vectorial transport of sodium from the apical to the basolateral surface (67,132,214,216,217,228,238). The active transport of sodium by type II cells appears to provide a major driving force for removal of fluid from the alveolar space.…”

Section: A Structural Features Of the Distal Pulmonary Epitheliamentioning

confidence: 99%

“…In situ hybridization studies, as well as Northern blot analyses done in mice, rats, and humans, have identified the presence of mRNA for all three subunits of ENaC in alveolar epithelial type II cells both in vivo and in vitro with usually a greater expression of ␣-than ␤-and ␥-subunits (64,75,78,162,220,223,232,238,264,315,345,348). The relative amounts of ENaC mRNA could explain the difference in ENaC activity and amiloride sensitivity between tissues and species, although a direct relationship between mRNA and functional protein cannot be predicted.…”

Section: Amiloride-sensitive Sodium Channels and Enacmentioning

confidence: 99%

Lung Epithelial Fluid Transport and the Resolution of Pulmonary Edema

Matthay

Folkesson²,

Clérici³

2002

Physiological Reviews

Self Cite

610

649

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The discovery of mechanisms that regulate salt and water transport by the alveolar and distal airway epithelium of the lung has generated new insights into the regulation of lung fluid balance under both normal and pathological conditions. There is convincing evidence that active sodium and chloride transporters are expressed in the distal lung epithelium and are responsible for the ability of the lung to remove alveolar fluid at the time of birth as well as in the mature lung when pathological conditions lead to the development of pulmonary edema. Currently, the best described molecular transporters are the epithelial sodium channel, the cystic fibrosis transmembrane conductance regulator, Na+-K+-ATPase, and several aquaporin water channels. Both catecholamine-dependent and -independent mechanisms can upregulate isosmolar fluid transport across the distal lung epithelium. Experimental and clinical studies have made it possible to examine the role of these transporters in the resolution of pulmonary edema.

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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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Rat lung alveolar type II cell line maintains sodium transport characteristics of primary culture

Cited by 14 publications

References 30 publications

Increased Virulence of a Fibronectin-Binding Protein Mutant of Staphylococcus aureus in a Rat Model of Pneumonia

Increased Virulence of a Fibronectin-Binding Protein Mutant of Staphylococcus aureus in a Rat Model of Pneumonia

Lung Epithelial Fluid Transport and the Resolution of Pulmonary Edema

Mechanisms of pulmonary edema clearance

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