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
| Autor: | Fadela Yebdri, Mohammed Chems-Eddine Smahi, Sara Dahou, Souheila Benmansour, Wafa Nouari, Mohammed Yassine Laoufi, Lamia Ysmail-Dahlouk, Maroua Miliani, Mourad Aribi, Zoheir Dahmani, Nassima Fakir, Amina Tourabi, Mouad Chaib-Draa |
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| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Staphylococcus aureus Necrosis Cell Survival Immunology Interleukin-1beta Ascorbic Acid Nitric Oxide Umbilical vein Nitric oxide 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Downregulation and upregulation medicine Human Umbilical Vein Endothelial Cells Immunology and Allergy Humans Immunologic Factors Cells Cultured Pharmacology ICAM-1 Interleukin-6 Staphylococcal Infections Ascorbic acid Intercellular Adhesion Molecule-1 Molecular biology Anti-Bacterial Agents Arginase 030104 developmental biology chemistry 030220 oncology & carcinogenesis cardiovascular system medicine.symptom Ex vivo |
| Zdroj: | International immunopharmacology. 95 |
| ISSN: | 1878-1705 |
| Popis: | Background Vitamin C (ascorbic acid, AscH2) has been shown to enhance immunity. Here, we studied its immunomodulatory effect on human endothelial cells (ECs) during S. aureus infection. Materials and methods The ex vivo effects of AscH2 were performed on primary human umbilical vein endothelial cells (HUVECs) infected or not with S. aureus. Results AscH2 treatment induced a marked downregulation of nitric oxide (NO) production and a moderate upregulation of arginase activity in S. aureus-infected HUVECs (respectively, p 0.05). Although the upregulated release levels of soluble intercellular adhesion molecular 1 (sICAM-1/sCD54) and sE-selectin (sCD62E) molecules were not significantly different between treated and untreated S. aureus-infected HUVECs, AscH2 treatment induced reversing effect on sICAM-1 release when comparing to uninfected control HUVECs. Moreover, AscH2 treatment appears to have a significant effect on preventing HUVEC necrosis induced by S. aureus infection (p 0.05). Additionally, S. aureus infection markedly downregulated total bound calcium ions (bCa2+) levels as compared to control HUVECs, whereas, AscH2 treatment induced a slight upregulation of bCa2+ levels in infected HUVECs as compared to infected and untreated HUVECs (p > 0.05). On the other hand, AscH2 treatment downregulated increased total cellular cholesterol content (tccCHOL) levels in HUVECs induced by S. aureus infection (p 0.05, and p Conclusions Our outcomes demonstrated that, during S. aureus infection, AscH2 treatment promotes human ECs survival and function, as well as prevents inflammatory response exacerbation, while inducing bactericidal activity. |
| Databáze: | OpenAIRE |
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