Sphingosine-1-phosphate increases human alveolar epithelial IL-8 secretion, proliferation and neutrophil chemotaxis

Milara, Javier; Mata, Manuel; Mauricio, Maria D.; Donet, Eva; Morcillo, Esteban J.; Cortijo, Julio

doi:10.1016/j.ejphar.2009.03.012

Cited by 41 publications

(31 citation statements)

References 31 publications

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“…In previous studies, sphingosin1-phosphate as a pro-inflammatory airway agent was able to induce ICAM-1 expression but failed to promote VCAM-1 induction in alveolar epithelial cells A549. This process was Ca 2+ -dependent, as tested by treatment with BAPTA-AM [40]. Dkk1 blocked diffusible Wnt-3 and thus indirectly increased VCAM-1 expression on bone marrow cells Fig.…”

Section: Discussionmentioning

confidence: 99%

Human placenta-derived Wnt-5a induces the expression of ICAM-1 and VCAM-1 in CD133+CD34+-hematopoietic progenitor cells

Herr

Horndasch

Howe

et al. 2014

Reproductive Biology

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Section: Discussionmentioning

confidence: 99%

Human placenta-derived Wnt-5a induces the expression of ICAM-1 and VCAM-1 in CD133+CD34+-hematopoietic progenitor cells

Herr

Horndasch

Howe

et al. 2014

Reproductive Biology

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“…These authors concluded that chemotaxis is decreased in isolated neutrophils from COPD patients versus healthy subjects and that the increased number of neutrophils in the airways of COPD patients may be related to the increase in neutrophil chemotactic factors in the lungs such as IL-8 or by the increase in adhesion molecules expression on pulmonary endothelial cells which is present in COPD patients [26,27,28]. In this work, we selected the Boyden chamber technique to measure neutrophil chemotaxis, since this is a well-experimented technique known for long by our group and others [18,19,29], and do not need to introduce nor manipulate cells with fluorescent dye incubations such as fluorescence calcein [26] which could modify neutrophil properties. In this line, there are few works that have studied peripheral blood chemotaxis in COPD patients versus healthy subjects, so discrepancy between previous observations and results shown in this study may be explained by different methods used to quantify chemotaxis and by differences in COPD patients, as the severe, early-onset patients in our study present a more advanced disease and therefore a possibly different neutrophil activation status.…”

Section: Discussionmentioning

confidence: 99%

Neutrophil Activation in Severe, Early-Onset COPD Patients versus Healthy Non-Smoker Subjects in vitro: Effects of Antioxidant Therapy

Milara¹,

Juan²,

Peiró³

et al. 2011

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Background: Neutrophils and oxidative stress have been implicated in the pathogenesis of COPD. Severe, early-onset COPD is characterized by a rapid decline in the lung function at an early age; however, nothing is known about neutrophil activation in COPD patients. Objectives: The aim of this study was to evaluate peripheral blood neutrophil activation in severe, early-onset COPD patients versus healthy non-smokers and the effect of N-acetyl-L-cysteine (NAC) on neutrophil activation in vitro. Methods: Neutrophils were isolated from 15 severe, early-onset COPD patients and 15 age-matched healthy subjects and stimulated with N-formyl- Met-Leu-Phe (fMLP) in the presence or absence of NAC (10 µM to 10 mM). Neutrophil chemotaxis, elastase release, reactive oxygen species (ROS), intracellular thiols and apoptosis were measured by Boyden chamber, spectrofluorometry, CMFDA and H₂DCF-DA dyes and by annexin V-FITC, respectively. Results: Chemotaxis of peripheral blood neutrophils from COPD patients in response to fMLP was 30% more increased than that observed in healthy subjects. Elastase release in response to fMLP was 2-fold higher in neutrophils from COPD patients versus healthy subjects. Intracellular thiol levels were 30% lower in COPD and ROS was approximately 30% higher in COPD versus healthy neutrophils. Spontaneous apoptosis showed no differences in both groups of patients and fMLP-induced apoptosis was higher in COPD. Pre-treatment with the antioxidant NAC effectively attenuated neutrophil chemotaxis, elastase release and ROS as well as effectively increased thiol levels in COPD. Conclusions: Neutrophils in severe, early-onset COPD patients are highly activated and this is alleviated by NAC in vitro.

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“…High local S1P concentrations may boost inflammation by augmenting PGE 2 release, inducing adhesion molecules, recruiting neutrophils [89,90] and monocyte/macrophages [91], retaining T-cells at sites of inflammation [87] and promoting activation of dendritic cells in the lymphatics [29]. At the same time, S1P may limit the local inflammatory response in a negative feedback manner by decreasing endothelial permeability, enhancing barrier function, and inhibiting leukocyte adhesion.…”

Section: Inflammationmentioning

confidence: 99%

Endothelial Functions of Sphingosine-1-phosphate

Lucke

Levkau

2010

Cell Physiol Biochem

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The biologically active sphingolipid sphingosine-1-phosphate (S1P) plays key functions in the immune, inflammatory, and cardiovascular systems. In the vasculature, S1P and its receptors are involved in vessel morphogenesis and angiogenesis during embryonic development and in the adult organism both under normal and pathological conditions. Via its actions on endothelial and smooth muscle cells, S1P regulates arterial tone, vascular permeability, and tissue perfusion. Elevated local S1P levels during inflammation induce endothelial adhesion molecules, recruit inflammatory cells, and activate dendritic cells. At the same time, S1P activates a negative feedback loop that consecutively seals endothelial cell-cell contacts, decreases vascular leakage, and inhibits cytokine-induced leukocyte adhesion. Thus S1P determines not only the build-up, magnitude, and duration of an inflammatory reaction but also the pace of its resolution. This review focuses on the role S1P plays in endothelial function, its receptors and signalling pathways, and the role its major carrier high-density lipoproteins (HDL) play in its bioavailability and transport. We will also discuss the potential of interfering with S1P-S1P receptor interactions for the treatment of endothelial disorders and vascular pathologies.

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Sphingosine-1-phosphate increases human alveolar epithelial IL-8 secretion, proliferation and neutrophil chemotaxis

Cited by 41 publications

References 31 publications

Human placenta-derived Wnt-5a induces the expression of ICAM-1 and VCAM-1 in CD133+CD34+-hematopoietic progenitor cells

Human placenta-derived Wnt-5a induces the expression of ICAM-1 and VCAM-1 in CD133+CD34+-hematopoietic progenitor cells

Neutrophil Activation in Severe, Early-Onset COPD Patients versus Healthy Non-Smoker Subjects in vitro: Effects of Antioxidant Therapy

Endothelial Functions of Sphingosine-1-phosphate

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