Effect of Escherichia coli lipopolysaccharide on phosphatidylcholine biosynthesis by rat lung and alveolar type II cells

Bosch, María Asunción; Risco, Cristina; Martin-Municio, Angel

doi:10.1007/bf00226188

Cited by 9 publications

(5 citation statements)

References 15 publications

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“…One is that LPS induces a reduction in the synthesis of PC. In lung tissue it is reported that LPS induces a reduction in pulmonary surfactant (PC) synthesis [14,15]. However, we found no evidence to support this possibility in the stomach, as both of the primary biosynthetic pathways for PC synthesis in our hands were unaffected by LPS at the dose and times used (Table 2).…”

Section: Discussioncontrasting

confidence: 62%

“…Also, a possible role for gastric alkalinization in gastric injury was approached by use of the proton pump inhibitor omeprazole. Because LPS has been implicated in causing inhibition of PC synthesis in another system, i.e., lung [14,15], we further investigated the de novo synthesis of PC in the stomach and the effect on it of LPS. Finally, we tested by surgical manipulation (pylorus ligation) the importance of duodenogastric reflux of intestinal contents on PC levels altered by LPS.…”

Section: Introductionmentioning

confidence: 99%

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Endotoxin-induced changes in phospholipid dynamics of the stomach

Dial

Tran

Hyman

et al. 2013

Journal of Surgical Research

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Background The gastric mucosa is protected in part by a hydrophobic layer of phosphatidylcholine (PC) that overlies the mucus gel on the stomach. Endotoxin treatment (i.e., lipopolysaccharide or LPS) results in an apparent disruption of this layer as evidenced by a reduction in surface hydrophobicity and an increase in transmural permeability. The current studies compared PC and lyso-PC levels in mucus and gastric mucosa before and after LPS treatment, and examined potential mechanisms for surface phospholipid changes. Methods Rats were administered LPS (5 mg//kg, ip) and samples were collected after 5 h for analysis of PC and its primary degradant, lyso-PC, in the loosely and firmly adherent mucus layers, and the mucosa. The dependence of LPS-induced effects on gastric alkalinization, PC synthetic activity, and intestinal reflux material was assessed. Results The gastric contents after LPS, which also contained duodenal reflux material, had greatly increased amounts of PC and lyso-PC. The firmly adherent mucus layer was unchanged. The gastric mucosa after LPS revealed significant reductions of PC levels and no change in lyso-PC content. These phospholipid changes were not caused by alkalinization of the stomach or altered PC synthesis. Prevention of duodenogastric reflux by pylorus ligation blocked the LPS-induced increase in luminal lyso-PC and the reduction in mucosal PC. Conclusions LPS appears to induce a release of PC from gastric mucosa into the lumen, along with degradation of PC to lyso-PC, without an affect on PC synthesis. Component(s) of intestinal reflux material appear to be required for these effects. The lowered PC levels in gastric mucosa after LPS may contribute to reduced barrier properties of this tissue.

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Section: Discussioncontrasting

confidence: 62%

Section: Introductionmentioning

confidence: 99%

Endotoxin-induced changes in phospholipid dynamics of the stomach

Dial

Tran

Hyman

et al. 2013

Journal of Surgical Research

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“…Part of our studies have been focussed on the interaction of LPS (from E. coli 0111:B4) with isolated rat type I1 pneumocytes, whose metabolism, in particular the biosynthesis of phospholipids, is disrupted in endotoxemic rats and also by treatment of cells with LPS in vitro (Aracil et al, 1985: Bosch et al, 1990. For studying the distribution of the endotoxin at different times of treatment, immunogold labeling was performed on Lowicryl K4M sections of isolated pneumocytes incubated with LPS at 37°C during 15,25,40,60, 90, and 120 min.…”

Section: Visualization Of the Endotoxin Interaction With Target Cellsmentioning

confidence: 99%

“…(Modified from Risco et al, 1993a, with permission of Journal ofEZectron Microscopy, Center for Academic Publications Japan.) important is the impairment of the metabolic routes of type I1 pneumocytes that are probably unable to replace the surfactant lost (Bosch et al, 1990). Studies performed in vivo showed that endotoxins reach the alveolar regions and accumulate in alveolar macro-phages, also entering the endothelial and epithelial cells (Freudenberg et al, 1984).…”

Section: Visualization Of the Endotoxin Interaction With Target Cellsmentioning

confidence: 99%

Cellular functions during activation and damage by pathogens: Immunogold studies of the interaction of bacterial endotoxins with target cells

Risco

Silva

1995

Microscopy Res & Technique

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Bacterial endotoxins (lipopolysaccharides or LPS) are active components of Gram-negative bacteria that act on numerous cellular functions through the processes of cell activation and damage. The molecular mechanisms involved in the "endotoxic phenomenon" are not defined yet, although extensive studies have been carried out. Immunogold and electron microscopy (EM) have contributed to identify the primary target cells of endotoxins and the subcellular systems that receive the direct action of these bacterial agents. Here, we review our studies on immunogold detection of endotoxins in cellular and subcellular systems. The analysis of the interaction between endotoxins and cells was focussed on the following aspects: (1) morphological characteristics of the LPS aqueous suspensions used in experimental work; (2) binding of endotoxins to the plasma membrane of type II pneumocytes and alveolar macrophages (two of their cellular targets), and influence of the state of aggregation of the LPS; (3) movement and distribution of endotoxins inside the cell, from the plasma membrane to the nucleoplasm; and (4) interaction of LPS with microtubules and its effects on the integrity of the microtubular network. These approaches provide information at the molecular level as well as data for the establishment of physiological models of endotoxicity.

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“…The microcirculatory disturbances with subsequent cellular injury and loss of organ function induced by LPS in intact animals have been attributed to the activation of inflammatory cells and strong inflammatory mediator generation. ATII exposed to LPS demonstrated a marked depression of surfactant synthesis and ion transport as well as strong up-regulation of adhesion molecules, cytokines such as TNF-␣, and NO synthesis via NO synthase II (NOSII) (11)(12)(13)(14).…”

mentioning

confidence: 99%

Apical, But Not Basolateral, Endotoxin Preincubation Protects Alveolar Epithelial Cells Against Hydrogen Peroxide-Induced Loss of Barrier Function: The Role of Nitric Oxide Synthesis

Rose

Guthmann

Tenenbaum

et al. 2002

The Journal of Immunology

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The influence of LPS preincubation on hydrogen peroxide (H2O2)-induced loss of epithelial barrier function was investigated in rat alveolar epithelial type II cells (ATII). Both apical and basolateral H2O2 administration caused a manyfold increase in transepithelial [3H]mannitol passage. Apical but not basolateral preincubation of ATII with LPS did not influence control barrier properties but fully abrogated the H2O2-induced leakage response. The effect of apical LPS was CD14 dependent and was accompanied by a strong up-regulation of NO synthase II mRNA and protein and NO release. Inhibition of NO by NG-monomethyl-l-arginine suppressed the LPS effect, whereas it was reproduced by exogenous application of gaseous NO or NO donor agents. Manipulation of the glutathione homeostasis (buthionine-(S,R)-sulfoximine) and the cGMP pathway (1H-(1,2,4)oxadiazolo[4,3-α]quinoxaline-1-one; zaprinast) did not interfere with the protective effect of LPS. Superoxide (O⨪2) generation by ATII cells was reduced by exogenous NO and LPS preincubation. O⨪2 scavenging with exogenous superoxide dismutase, the intracellular superoxide dismutase analog Mn(III)tetrakis(4-benzoic acid) porphyrin, and the superoxide scavenger nitroblue tetrazolium and, in particular, hydroxyl radical scavenging with hydroxyl radical scavenger 1,3-dimethyl-thiourea inhibited the H2O2-induced epithelial leakage response. In conclusion, apical but not basolateral LPS preincubation of ATII cells provides strong protection against H2O2-induced transepithelial leakage, attributable to an up-regulation of epithelial NO synthesis. It is suggested that the LPS-induced NO formation is effective via interaction with reactive oxygen species, including superoxide and hydroxyl radicals. The polarized epithelial response to LPS may be part of the lung innate immune system, activated by inhaled endotoxin or under conditions of pneumonia.

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Effect of Escherichia coli lipopolysaccharide on phosphatidylcholine biosynthesis by rat lung and alveolar type II cells

Cited by 9 publications

References 15 publications

Endotoxin-induced changes in phospholipid dynamics of the stomach

Endotoxin-induced changes in phospholipid dynamics of the stomach

Cellular functions during activation and damage by pathogens: Immunogold studies of the interaction of bacterial endotoxins with target cells

Apical, But Not Basolateral, Endotoxin Preincubation Protects Alveolar Epithelial Cells Against Hydrogen Peroxide-Induced Loss of Barrier Function: The Role of Nitric Oxide Synthesis

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