Imène Belhassena1, Wafa Nouari1, Aida Messaoud1, Mouna Nouar1, Mohamed Brahimi2, Sid-Ahmed Chawki Lamara3, Mourad Aribi4. 1. Laboratory of Applied Molecular Biology and Immunology, BioMolIm, W0414100, University of Tlemcen, 13000 Tlemcen, Algeria. 2. EHU "1er Novembre 1954" - Hemobiology, Oran, Algeria. 3. Department of Biotechnology, University of Oran, 1 Ahmed Ben Bella, 31000 Oran, Algeria. 4. Laboratory of Applied Molecular Biology and Immunology, BioMolIm, W0414100, University of Tlemcen, 13000 Tlemcen, Algeria. Electronic address: mourad.aribi@univ-tlemcen.dz.
Abstract
BACKGROUND: Exacerbation of CD16 as molecule marker of both intermediate and non-classical monocytes (MOs) has been shown to be involved in the pathogenesis of myocardial infarction (MI). In this study, we have tried to evaluate the aspirin (acetylsalicylic acid, ASA) treatment effect on the CD16-expressed MOs and activation-associated CD40 in MI. METHODS: MOs were isolated from the whole blood of healthy controls and patients with MI. The cells were stimulated and treated with different doses of ASA. RESULTS: ASA significantly decreased nitric oxide (NO) production and inducible NO synthase (iNOS) activity, but significantly increased arginase activity. Levels of interleukin (IL)-1β, IL-6 and interferon-γ (IFN-γ) were downregulated, whereas those of IL-10 were upregulated. Additionally, ASA induced a markedly increase in both phagocytosis and intracellular pathogen killing activities. Moreover, ASA treatment induced significantly upregulation of intracellular levels of glucose (iGlu), and free calcium ions (ifCa2+), and, covertly, significantly downregulation of total cellular cholesterol content (tccCHOL). Furthermore, the expression levels of CD16 and CD40 were significantly downregulated in ASA-treated MOs. CONCLUSIONS: We show for the first time that ASA immunomodulates the functional activities of MOs during MI and promotes their switching toward a classical phenotype, exhibiting low CD16 expression levels and thereby anti-inflammatory properties.
BACKGROUND: Exacerbation of CD16 as molecule marker of both intermediate and non-classical monocytes (MOs) has been shown to be involved in the pathogenesis of myocardial infarction (MI). In this study, we have tried to evaluate the aspirin (acetylsalicylic acid, ASA) treatment effect on the CD16-expressed MOs and activation-associated CD40 in MI. METHODS: MOs were isolated from the whole blood of healthy controls and patients with MI. The cells were stimulated and treated with different doses of ASA. RESULTS:ASA significantly decreased nitric oxide (NO) production and inducible NO synthase (iNOS) activity, but significantly increased arginase activity. Levels of interleukin (IL)-1β, IL-6 and interferon-γ (IFN-γ) were downregulated, whereas those of IL-10 were upregulated. Additionally, ASA induced a markedly increase in both phagocytosis and intracellular pathogen killing activities. Moreover, ASA treatment induced significantly upregulation of intracellular levels of glucose (iGlu), and free calcium ions (ifCa2+), and, covertly, significantly downregulation of total cellular cholesterol content (tccCHOL). Furthermore, the expression levels of CD16 and CD40 were significantly downregulated in ASA-treated MOs. CONCLUSIONS: We show for the first time that ASA immunomodulates the functional activities of MOs during MI and promotes their switching toward a classical phenotype, exhibiting low CD16 expression levels and thereby anti-inflammatory properties.