<b>Synthesis and release of phosphatidylcholine by isolated porcine gastric mucous cells in primary culture</b>

Background-Gastric mucosal surface hydrophobicity (GMSH) is an essential component of the mucosal defence system that is decreased by Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs). Gastric ulcers occur predominantly in elderly subjects, and may thus reflect diminished mucosal resistance. Aims-To investigate whether aging decreases GMSH. Patients-One hundred and twenty patients without peptic ulcer disease were divided into three age groups: I (41 years or below); II (41-64 years); and III (65 years or above). Methods-Biopsy specimens were taken from the antrum, corpus, and cardia for histology (Sydney system), urease testing for H pylori, and for contact angle measurement of GMSH with a goniometer. The presence of specific H pylori antibodies was checked by immunoblotting. Results-Fifty two patients (43%) were infected, and 68 were uninfected with H pylori. GMSH at all biopsy sites was lower in H pylori infected subjects (p=0.0001), but also decreased with age independently of infection status (p=0.0001). The most notable decrease in GMSH occurred between age groups I and II in those with, and between age groups II and III in those without, H pylori infection. GMSH was greater in antral than in corpus mucosa in both infected (p=0.0001) and uninfected patients (p=0.0003). Conclusions-A physiological decrease in GMSH with aging may contribute to the risk of ulcer development in the elderly, and may act synergistically with H pylori and/or NSAIDs on gastric mucosal defence. (Gut 1998;43:465-469)

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“…30 In the rat and canine gastric mucosa PGE 2 has been shown to increase hydrophobicity and reverse the hydrophobicity reduced by aspirin 31-33…”

Section: Discussionmentioning

confidence: 99%

Age and Helicobacter pylori decrease gastric mucosal surface hydrophobicity independently

Hackelsberger

Platzer

Nilius

et al. 1998

Gut

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“…Comparison with other cell types that actively secrete PL, such as hepatocytes, type II alveolar cells, and gastric mucosal cells may prove useful in this regard. PL is secreted by hepatocytes both in bile and in lipoprotein complexes (31,32), and by the gastric mucosa to form a protective hydrophobic barrier (23,33). In all cases, although a degree of molecular species selectivity has been demonstrated in these regulated secretion processes, the PC species secreted were always also major components of the total cellular PL extract.…”

Section: Surface Activity Of Surf Trachasp Surf Bal and Surf P27000mentioning

confidence: 99%

Conductive Airway Surfactant: Surface-tension Function, Biochemical Composition, and Possible Alveolar Origin

Bernhard

Tschernig

et al. 1997

Am J Respir Cell Mol Biol

113

124

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Alveolar surfactant is well known for its ability to reduce minimal surface tension at the alveolar air-liquid interface to values below 5 mN/m. In addition, it has been suggested that an analogous conductive airway surfactant is also present in the airways. To elucidate the composition, possible origin, and surface activity of conductive airway phospholipids (PL), we compared in adult porcine lungs the PL classes and phosphatidylcholine (PC) molecular species of nonpurified tracheal aspirate samples with those of bronchoalveolar lavage fluid (BAL), tracheobronchial epithelium, and lung parenchyma. We also analyzed PL and PC composition, protein content, and surface activity of surfactant isolated from tracheal aspirates (SurfTrachAsp), BAL (SurfBAL), and the 27,000 x g pellet of BAL (SurfP27000) by density-gradient centrifugation. Although PL composition revealed contributions of the airways to tracheal aspirates, the composition of PC molecular species of tracheal aspirates was similar to that of BAL and lung parenchyma, but differed considerably from that of airway epithelium. SurfTrachAsp had the same PL and PC composition as SurfBAL and SurfP27000, indicating that this fraction of tracheal aspirates may have originated from the alveoli. Nevertheless, minimal and maximal surface tensions were higher in SurfTrachAsp than in SurfBAL and SurfP27000. Analysis of surfactant proteins A, B, and C (SP-A, SP-B, and SP-C) revealed that SP-A was decreased and SP-B and SP-C were absent, whereas total protein was increased in SurfTrachAsp. We conclude that as compared with alveolar surfactant, PL of SurfTrachAsp show the same composition, but that surface-tension function is impaired and the concentration of surfactant proteins is decreased in SurfTrachAsp.

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“…We used a labeling time of 3 h to investigate the PL metabolism of isolated tracheae compared with lungs. This ensured morphological and metabolic integrity of the organs, and from other studies using isolated organs or cells, linear incorporation of [methyl-3 H]choline over 6-24 h can be assumed (12,39). Because of the rapid turnover of plasma choline in vivo (15), however, incorporation of [methyl-3 H]choline into lung tissue PC reaches a plateau after 3 h; this plateau is maintained for Ն24 h in in vivo experiments using mice (37).…”

Section: Discussionmentioning

confidence: 81%

Phosphatidylcholine metabolism of rat trachea in relation to lung parenchyma and surfactant

Rau¹,

Dombrowsky²,

Gebert³

et al. 2003

Journal of Applied Physiology

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Pulmonary surfactant prevents alveolar collapse and contributes to airway patency by reducing surface tension. Although alveolar surfactant, consisting mainly of phospholipids (PL) together with neutral lipids and surfactant-specific proteins, originates from type II pneumocytes, the contribution of airway epithelia to the PL fraction of conductive airway surfactant is still debated. We, therefore, analyzed the composition, synthesis, and release of phosphatidylcholine (PC) molecular species as the main surfactant PL of the rat trachea compared with the lung. Analyses of individual PC molecular species with HPLC and electrospray ionization mass spectrometry revealed that the rat trachea contained and synthesized much more palmitoyloleoyl-PC, palmitoyllinoleoyl-PC, and palmitoylarachidonoyl-PC, together with increased amounts of alkylacyl-PC, and less surfactant-specific species such as dipalmitoyl-PC than the lung. Organ cultures with [methyl-3H]choline as precursor of PC revealed that, in the trachea, synthesized PC was retained in the tissue, rather than secreted. [Methyl-3H]choline-labeled dipalmitoyl-PC was a negligible component in the trachea, and, in contrast to the lungs, palmitoyloleoyl-PC was enriched in tracheal secretions. We conclude that the surfactant fraction in the airways does not originate from the airways but is produced in the alveolar space and transported upward.

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Synthesis and release of phosphatidylcholine by isolated porcine gastric mucous cells in primary culture

Cited by 6 publications

References 13 publications

Age and Helicobacter pylori decrease gastric mucosal surface hydrophobicity independently

Age and Helicobacter pylori decrease gastric mucosal surface hydrophobicity independently

Conductive Airway Surfactant: Surface-tension Function, Biochemical Composition, and Possible Alveolar Origin

Phosphatidylcholine metabolism of rat trachea in relation to lung parenchyma and surfactant

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