Interleukin-8 Release by Endothelial Colony-Forming Cells Isolated from Idiopathic Pulmonary Fibrosis Patients Might Contribute to Their Pathogenicity

Blandinières, Adeline; Gendron, Nicolas; Bacha, N.; Bièche, Ivan; Nunès, H.; Névo, Nathalie; Rossi, Elisa; Crestani, Bruno; Lecourt, S.; Chevret, Sylvie; Lokajczyk, Anna; Kisaoglu, A.; Juvin, Karine; Bertil, Sébastien; Valeyre, D; Cras, Audrey; Gaussem, Pascale; Israël‐Biet, Dominique; Smadja, David

doi:10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5410

Cited by 3 publications

(3 citation statements)

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“…33 Recently, a prospective study also demonstrated that excess PMNs in the blood of IPF patients also predicted worse outcomes and that this enhanced neutrophilia may occur because endothelial colony-forming cells isolated from IPF patients secreted IL-8/CXCL8, a known PMN-recruiting chemokine. 34 This study also noted PMNs present in histologic analyses of IPF lungs. Excessive PMN degranulation or necrosis can lead to the release of many proteolytic enzymes including NE.…”

Section: Innate Immune Cells and The Pathogenesis Of Lung Fibrosis Posupporting

confidence: 61%

A pathologic two‐way street: how innate immunity impacts lung fibrosis and fibrosis impacts lung immunity

2019

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Lung fibrosis is characterised by the accumulation of extracellular matrix within the lung and is secondary to both known and unknown aetiologies. This accumulation of scar tissue limits gas exchange causing respiratory insufficiency. The pathogenesis of lung fibrosis is poorly understood, but immunologic‐based treatments have been largely ineffective. Despite this, accumulating evidence suggests that innate immune cells and receptors play important modulatory roles in the initiation and propagation of the disease. Paradoxically, while innate immune signalling may be important for the pathogenesis of fibrosis, there is also evidence to suggest that innate immune function against pathogens may be impaired, leading to dysregulated and/or impaired host defence. This review summarises the evidence for this pathologic two‐way street, highlights new concepts of pathogenesis and recommends future directions for research emphasis.

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Section: Innate Immune Cells and The Pathogenesis Of Lung Fibrosis Posupporting

confidence: 61%

A pathologic two‐way street: how innate immunity impacts lung fibrosis and fibrosis impacts lung immunity

2019

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“…The pathogenic pathways involved in the local lung fibrogenesis, in particular in idiopathic pulmonary fibrosis (IPF), are still elusive. However, lung parenchymal lesions are consistently associated with major vascular remodeling processes, 2 microvascular alterations, 3 and changes in endothelial phenotype 4–6 . Mechanisms underlying this vascular remodeling are yet to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

Placental growth factor level in plasma predicts COVID‐19 severity and in‐hospital mortality

Smadja

Philippe

Bory

et al. 2021

Journal of Thrombosis and Haemostasis

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Background Coronavirus disease 2019 (COVID‐19) is a respiratory disease associated with vascular inflammation and endothelial injury. Objectives To correlate circulating angiogenic markers vascular endothelial growth factor A (VEGF‐A), placental growth factor (PlGF), and fibroblast growth factor 2 (FGF‐2) to in‐hospital mortality in COVID‐19 adult patients. Methods Consecutive ambulatory and hospitalized patients with COVID‐19 infection were enrolled. VEGF‐A, PlGF, and FGF‐2 were measured in each patient ≤48 h following admission. Results The study enrolled 237 patients with suspected COVID‐19: 208 patients had a positive diagnostic for COVID‐19, of whom 23 were mild outpatients and 185 patients hospitalized after admission. Levels of VEGF‐A, PlGF, and FGF‐2 significantly increase with the severity of the disease (P < .001). Using a logistic regression model, we found a significant association between the increase of FGF‐2 or PlGF and mortality (odds ratio [OR] 1.11, 95% confidence interval [CI; 1.07–1.16], P < .001 for FGF‐2 and OR 1.07 95% CI [1.04–1.10], P < .001 for PlGF) while no association were found for VEGF‐A levels. Receiver operating characteristic curve analysis was performed and we identified PlGF above 30 pg/ml as the best predictor of in‐hospital mortality in COVID‐19 patients. Survival analysis for PlGF confirmed its interest for in‐hospital mortality prediction, by using a Kaplan‐Meier survival curve (P = .001) and a Cox proportional hazard model adjusted to age, body mass index, D‐dimer, and C‐reactive protein (3.23 95% CI [1.29–8.11], P = .001). Conclusion Angiogenic factor PlGF is a relevant predictive factor for in‐hospital mortality in COVID‐19 patients. More than a biomarker, we hypothesize that PlGF blocking strategies could be a new interesting therapeutic approach in COVID‐19.

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“…83 84 Using galactosidase staining, annexin-V staining, and p16 expression measurement of ECFCs, increased endothelial senescent and apoptotic states were shown for IPF patients. 85…”

Section: Potential Use Of Ecfcs For Diagnostic Purposesmentioning

confidence: 99%

Potentials of Endothelial Colony-Forming Cells: Applications in Hemostasis and Thrombosis Disorders, from Unveiling Disease Pathophysiology to Cell Therapy

Schwarz,

Yadegari

2023

Hamostaseologie

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Endothelial colony-forming cells (ECFCs) are endothelial progenitor cells circulating in a limited number in peripheral blood. They can give rise to mature endothelial cells (ECs) and, with intrinsically high proliferative potency, contribute to forming new blood vessels and restoring the damaged endothelium in vivo. ECFCs can be isolated from peripheral blood or umbilical cord and cultured to generate large amounts of autologous ECs in vitro. Upon differentiation in culture, ECFCs are excellent surrogates for mature ECs showing the same phenotypic, genotypic, and functional features. In the last two decades, the ECFCs from various vascular disease patients have been widely used to study the diseases' pathophysiology ex vivo and develop cell-based therapeutic approaches, including vascular regenerative therapy, tissue engineering, and gene therapy. In the current review, we will provide an updated overview of past studies, which have used ECFCs to elucidate the molecular mechanisms underlying the pathogenesis of hemostatic disorders in basic research. Additionally, we summarize preceding studies demonstrating the utility of ECFCs as cellular tools for diagnostic or therapeutic clinical applications in thrombosis and hemostasis.

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Interleukin-8 Release by Endothelial Colony-Forming Cells Isolated from Idiopathic Pulmonary Fibrosis Patients Might Contribute to Their Pathogenicity

Cited by 3 publications

References 0 publications

A pathologic two‐way street: how innate immunity impacts lung fibrosis and fibrosis impacts lung immunity

A pathologic two‐way street: how innate immunity impacts lung fibrosis and fibrosis impacts lung immunity

Placental growth factor level in plasma predicts COVID‐19 severity and in‐hospital mortality

Potentials of Endothelial Colony-Forming Cells: Applications in Hemostasis and Thrombosis Disorders, from Unveiling Disease Pathophysiology to Cell Therapy

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