L-Threoascorbic acid treatment promotes S. aureus-infected primary human endothelial cells survival and function, as well as intracellular bacterial killing, and immunomodulates the release of IL-1β and soluble ICAM-1

Dahou, Sara; Smahi, M.; Nouari, Wafa; Dahmani, Zoheir; Benmansour, Souheila; Ysmail-Dahlouk, Lamia; Miliani, Maroua; Yebdri, Fadela; Fakir, Nassima; Laoufi, Mohammed Yassine; Chaib-Draa, Mouad; Tourabi, Amina; Aribi, Mourad

doi:10.1016/j.intimp.2021.107476

Cited by 4 publications

(4 citation statements)

References 120 publications

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“…ECs, apart from their vascular function, are now considered as relevant immunoregulatory effectors in chronic inflammatory diseases (82,83). Following cellular damage, ECs release large amount of IL-1b and IL-6 and increase the expression of adhesion molecules, like E-selectin (CD62E) and ICAM-1 (CD54), that further contribute to the exacerbate inflammation and trained immunity (80), including in ATS. In the case of ATS, the persistent activation of the inflammatory state, due to trained immunity, has been hypothesized as a relevant mechanisms linking non-resolving inflammation in ATS (84)(85)(86).…”

Section: Nk Cells In Atherosclerosismentioning

confidence: 99%

“…Upregulation of cell cholesterol is a relevant hallmark of the ATS plaque, exacerbating the pro-inflammatory state that impact on the plaque fate, by continuously damaging the ECs and SMCs, finally determining the plaque rupture. Of notice, upregulated cell cholesterol induce a signature of trained immunity ( 80 ). Trained immunity, a concept recently developed, refers to the ability of innate immunity to develop a specific memory as for adaptive immunity ( 17 ).…”

Section: Introductionmentioning

confidence: 99%

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When a Friend Becomes Your Enemy: Natural Killer Cells in Atherosclerosis and Atherosclerosis-Associated Risk Factors

et al. 2022

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Atherosclerosis (ATS), the change in structure and function of arteries with associated lesion formation and altered blood flow, is the leading cause of cardiovascular disease, the number one killer worldwide. Beyond dyslipidemia, chronic inflammation, together with aberrant phenotype and function of cells of both the innate and adaptive immune system, are now recognized as relevant contributors to atherosclerosis onset and progression. While the role of macrophages and T cells in atherosclerosis has been addressed in several studies, Natural Killer cells (NKs) represent a poorly explored immune cell type, that deserves attention, due to NKs’ emerging contribution to vascular homeostasis. Furthermore, the possibility to re-polarize the immune system has emerged as a relevant tool to design new therapies, with some succesfull exmples in the field of cancer immunotherapy. Thus, a deeper knowledge of NK cell pathophysiology in the context of atherosclerosis and atherosclerosis-associated risk factors could help developing new preventive and treatment strategies, and decipher the complex scenario/history from “the risk factors for atherosclerosis” Here, we review the current knowledge about NK cell phenotype and activities in atherosclerosis and selected atherosclerosis risk factors, namely type-2 diabetes and obesity, and discuss the related NK-cell oriented environmental signals.

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Section: Nk Cells In Atherosclerosismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

When a Friend Becomes Your Enemy: Natural Killer Cells in Atherosclerosis and Atherosclerosis-Associated Risk Factors

et al. 2022

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“…Many studies have confirmed that the endothelial cell immune response caused by bacteria is closely related to the inflammatory pathway proteins of HUVEC. 55 , 56 , 57 And bacterial adhesion to targets in endothelial cells may be a critical step in causing bacterial infection. It has been shown that Chlamydia Pneumoniae Cpn60 stimulates monocytes and induces metalloproteinase and pro-inflammatory cytokines synthesis.…”

Section: Discussionmentioning

confidence: 99%

CircTMEM165 facilitates endothelial repair by modulating mitochondrial fission via miR-192/SCP2 in vitro and in vivo

Liu,

Yang,

et al. 2024

iScience

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“…Thus, vitamin C can be a safe and natural alternative to limit the growth of S. aureus when non-toxicity is required [5]. Moreover, in addition to its well-known immunomodulatory effects, it has recently been shown to possess immunomodulatory properties opposing interesting endothelial cell infection [6].…”

Section: Introductionmentioning

confidence: 99%

Vitamin C preventsS. aureusinfections of endothelial cells through its interaction with specific residues in the active site of gC1qR/p33 involved in direct entry, notably SER230, ASN345, ILE348, TYR224, ASN346, SER347, and GLU438, and its potential inhibitory effects on FnBPs, α5β1, and Protein A molecules

Miliani,

Hadjidj,

Bensefia

et al. 2024

Preprint

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Staphylococcus aureus (S. aureus), often perceived as an extracellular pathogenic agent, exhibits a remarkable ability to penetrate host cells, including endothelial, epithelial, and osteoblastic cells, significantly contributing to the pathogenesis of infections. A significant pathway for this invasion appears to involve the bacterium's binding to the α5β1 integrin via a fibronectin bridge, followed by phagocytosis. Additionally, S. aureus presents staphylococcal protein A, a cell wall protein that binds to the Fc and Fab regions of immunoglobulins, playing a crucial role in virulence and immune evasion, and can also bind directly to the gC1qR receptor on endothelial cells. Furthermore, vitamin C is recognized for its antimicrobial and immunomodulatory properties, offering potential for reducing the risk of infection. Considering the aforementioned elements, our study focused on exploring the potential effects of vitamin C on the interactions between S. aureus and endothelial cells. Thus, we particularly examined two aspects: on the one hand, interactions involving fibronectin-binding proteins (FnBPs) proteins and human α5β1 integrin, and on the other hand, the interaction between vitamin C and the direct entry receptor (the globular heads of complement component 1q receptor [gC1qR/p33], also known as hyaluronic acid binding protein 1 [HABP1]). To achieve this, we utilized molecular modeling assays, primarily relying on molecular docking.

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L-Threoascorbic acid treatment promotes S. aureus-infected primary human endothelial cells survival and function, as well as intracellular bacterial killing, and immunomodulates the release of IL-1β and soluble ICAM-1

Cited by 4 publications

References 120 publications

When a Friend Becomes Your Enemy: Natural Killer Cells in Atherosclerosis and Atherosclerosis-Associated Risk Factors

When a Friend Becomes Your Enemy: Natural Killer Cells in Atherosclerosis and Atherosclerosis-Associated Risk Factors

CircTMEM165 facilitates endothelial repair by modulating mitochondrial fission via miR-192/SCP2 in vitro and in vivo

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