Surfactant
Ontology highlight
ABSTRACT:
SUBMITTER: Rimensberger P
PROVIDER: S-EPMC7175631 | biostudies-literature | 2013 Oct
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:Study the Role of Surfactant Protein C in Innate Lung Defense. Gene expression profiles comparison between isolated TYPE II cells from SPC(-/-) and control litter mates.
2012-08-21 | E-GEOD-35989 | biostudies-arrayexpress
Project description:Study the Role of Surfactant Protein C in Innate Lung Defense.
2012-08-21 | GSE35989 | GEO
Project description:Mutations in genes encoding proteins needed for normal surfactant function and metabolism cause acute lung disease in newborns and chronic lung disease in older children and adults. While rare these disorders are associated with considerable pulmonary morbidity and mortality. The identification of genes responsible for surfactant dysfunction provides clues for candidate genes contributing to more common respiratory conditions, including neonatal respiratory distress syndrome and lung diseases associated with aging or environmental insults. While clinical, imaging and histopathology features of these disorders overlap, certain features are distinctive for surfactant dysfunction. Natural histories differ depending upon the genes involved and a specific diagnosis is important to provide accurate information concerning prognosis and mode of inheritance. Diagnosis of surfactant dysfunction can be made by biopsy, but identification of the specific gene involved requires molecular genetic testing, which is non-invasive. Currently there are no effective medical treatments for surfactant dysfunction. Development of therapies is a priority for research, which may benefit patients with other lung diseases.
| S-EPMC3201772 | biostudies-literature
Project description:The amount of pulmonary surfactant within type II cells and in the alveolar space, referred to as surfactant pool sizes, are tightly regulated. The molecular pathways that sense and regulate surfactant pool size within the alveolus have not been identified and constitute a fundamental knowledge gap in the field. Our data show that mice with a germline mutation in the orphan G-protein-coupled receptor, GPR116, have a 30-fold accumulation of surfactant phospholipids that causes respiratory distress in adult animals. This phenotype is associated with increased surfactant secretion and induction of the purinergic receptor P2RY2 in young animals, and lipid-laden macrophages and alveolar destruction in older animals. We further demonstrate that GPR116 mRNA expression is developmentally regulated in the murine lung with peak expression at birth when surfactant pool sizes are maximal. Within the lung, GPR116 protein expression is restricted to the apical plasma membrane of alveolar type I and type II epithelial cells. To better understand the roles and molecular mechanisms by which Gpr116 influences gene expression in lung, the effect of cell-selective deletion of Gpr116 (Gpr116D/D) on genome-wide mRNA expression profiles was determined in murine type II alveolar epithelial cells. Differentially expressed genes were identified from Affymetrix Murine GeneChips analysis and subjected to gene ontology classification promoter analysis, pathway mapping and literature mining.
2013-04-10 | E-GEOD-41417 | biostudies-arrayexpress
Project description:The response of bacteria to the conditions at the site of infection is a key part of the transcriptional program that will determine the sucess of the infectious agent. To model the environment of the distal airway, we used bovine pulmonary surfactant (Survanta). P. aeruginosa transcript levels were measured in the presence or absence of Survanta in MOPS minimal medium to identify transcripts altered in response to surfactant. The most highly induced transcript in Survanta was PA5325, renamed sphA based on our findings that the gene was specifically induced by sphingosine derived from the sphingomyelin present in pulmonary surfactant. A divergently transcribed transcription factor, PA5324, was demonstrated to be critical for the sphingosine dependent induction of sphA and was therefore renamed SphR. Microarrays of the sphR mutant cells were compared to wild type to determine the likely SphR regulon. Wild type and sphR mutant cells were pre-grown in MOPS minimal media and then split and resuspended in MOPS pyruvate or MOPS pyruvate + surfactant
2013-12-10 | E-GEOD-48982 | biostudies-arrayexpress
Project description:When compressed by the shrinking alveolar surface area during exhalation, films of pulmonary surfactant in situ reduce surface tension to levels at which surfactant monolayers collapse from the surface in vitro. Vesicles of pulmonary surfactant added below these monolayers slow collapse. X-ray scattering here determined the structural changes induced by the added vesicles. Grazing incidence X-ray diffraction on monolayers of extracted calf surfactant detected an ordered phase. Mixtures of dipalmitoyl phosphatidylcholine and cholesterol, but not the phospholipid alone, mimic that structure. At concentrations that stabilize the monolayers, vesicles in the subphase had no effect on the unit cell, and X-ray reflection showed that the film remained monomolecular. The added vesicles, however, produced a concentration-dependent increase in the diffracted intensity. These results suggest that the enhanced resistance to collapse results from enlargement by the additional material of the ordered phase.
| S-EPMC8754419 | biostudies-literature
Project description:Environmental remediation efforts often utilize either biodegradative microbes or surfactants, but not in combination. Coupling both strategies holds the potential to dramatically increase the rate and extent of remediation because surfactants can enhance the bioavailability of contaminants to microbes. However, many surfactants permeabilize bacterial cell membranes and are effective disinfectants. An important goal then is to find or genetically modify microorganisms that possess both desirable degradative capabilities and the ability to thrive in the presence of surfactants. The guts of some marine invertebrates, particularly deposit feeders, have previously been shown to contain high levels of biosurfactants. Our primary aim was to mine these natural, surfactant-rich habitats for surfactant-resistant bacteria. Relative to sediment porewaters, the gut contents of two polychaete deposit feeders, Nereis succinea and Amphitrite ornata, exhibited a significantly higher ratio of bacteria resistant to both cationic and anionic surfactants. In contrast, bacteria in the gut fluids of a holothuroid, Leptosynapta tenuis, showed surfactant susceptibility similar to that of bacteria from sediments. Analyses of 16S rRNA gene sequences revealed that the majority of surfactant-resistant isolates were previously undescribed species of the genus Vibrio or were of a group most closely related to Spongiobacter spp. We also tested a subset of resistant bacteria for the production of biosurfactants. The majority did produce biosurfactants, as demonstrated via the oil-spreading method, but in all cases, production was relatively weak under the culture conditions employed. Novel surfactant-resistant, biosurfactant-producing bacteria, and the habitats from which they were isolated, provide a new source pool for potential microorganisms to be exploited in the in situ bioremediation of marine sediments.
| S-EPMC2519273 | biostudies-literature
Project description:The amount of pulmonary surfactant within type II cells and in the alveolar space, referred to as surfactant pool sizes, are tightly regulated. The molecular pathways that sense and regulate surfactant pool size within the alveolus have not been identified and constitute a fundamental knowledge gap in the field. Our data show that mice with a germline mutation in the orphan G-protein-coupled receptor, GPR116, have a 30-fold accumulation of surfactant phospholipids that causes respiratory distress in adult animals. This phenotype is associated with increased surfactant secretion and induction of the purinergic receptor P2RY2 in young animals, and lipid-laden macrophages and alveolar destruction in older animals. We further demonstrate that GPR116 mRNA expression is developmentally regulated in the murine lung with peak expression at birth when surfactant pool sizes are maximal. Within the lung, GPR116 protein expression is restricted to the apical plasma membrane of alveolar type I and type II epithelial cells.
2013-04-10 | GSE41417 | GEO
Project description:The response of bacteria to the conditions at the site of infection is a key part of the transcriptional program that will determine the sucess of the infectious agent. To model the environment of the distal airway, we used bovine pulmonary surfactant (Survanta). P. aeruginosa transcript levels were measured in the presence or absence of Survanta in MOPS minimal medium to identify transcripts altered in response to surfactant. The most highly induced transcript in Survanta was PA5325, renamed sphA based on our findings that the gene was specifically induced by sphingosine derived from the sphingomyelin present in pulmonary surfactant. A divergently transcribed transcription factor, PA5324, was demonstrated to be critical for the sphingosine dependent induction of sphA and was therefore renamed SphR. Microarrays of the sphR mutant cells were compared to wild type to determine the likely SphR regulon.
2013-12-10 | GSE48982 | GEO
Project description:BACKGROUND:Many premature infants with respiratory failure are deficient in surfactant, but the relationship to occurrence of bronchopulmonary dysplasia (BPD) is uncertain. METHODS:Tracheal aspirates were collected from 209 treated and control infants enrolled at 7-14 days in the Trial of Late Surfactant. The content of phospholipid, surfactant protein B, and total protein were determined in large aggregate (active) surfactant. RESULTS:At 24?h, surfactant treatment transiently increased surfactant protein B content (70%, p?<?0.01), but did not affect recovered airway surfactant or total protein/phospholipid. The level of recovered surfactant during dosing was directly associated with content of surfactant protein B (r?=?0.50, p?<?0.00001) and inversely related to total protein (r?=?0.39, p?<?0.0001). For all infants, occurrence of BPD was associated with lower levels of recovered large aggregate surfactant, higher protein content, and lower SP-B levels. Tracheal aspirates with lower amounts of recovered surfactant had an increased proportion of small vesicle (inactive) surfactant. CONCLUSIONS:We conclude that many intubated premature infants are deficient in active surfactant, in part due to increased intra-alveolar metabolism, low SP-B content, and protein inhibition, and that the severity of this deficit is predictive of BPD. Late surfactant treatment at the frequency used did not provide a sustained increase in airway surfactant.
| S-EPMC6377352 | biostudies-literature