OBJECTIVE: LDL(-) is a minor LDL subfraction that induces inflammatory factor release by endothelial cells. Since LDL(-) is present in plasma, its interaction with leucocytes, a cell type involved in atherosclerosis phenomena, is feasible; therefore, the aim of the current study was to evaluate LDL(-) effect on lymphocytes and monocytes isolated from human plasma. METHODS AND RESULTS: Mononuclear cells were incubated with LDL(+) and LDL(-) and expression and release of several inflammatory mediators were analyzed by protein membrane assay, ELISA and real-time RT-PCR. LDL(-) induced a significantly increased production versus LDL(+) in MCP1, GRObeta, GROgamma, IL6, IL8 and IL10 in monocytes as well as in lymphocytes. These induced molecules are inflammatory, except for IL10 which is considered an anti-inflammatory cytokine. Therefore, the role of IL10 was evaluated in experiments where exogenous IL10 or antibodies anti-IL10 or anti-IL10 receptor were added. IL10 addition diminished the release of the other factors induced by LDL(-) near to basal production both at protein and RNA level. In contrast, the antibody anti-IL10 increased inflammatory cytokine release around two-fold, whereas the antibody anti-IL10 receptor produced a lower effect. CONCLUSIONS: LDL(-) promoted inflammatory cytokine production in leucocytes; however, it also induced IL10 that minimized this effect. Therefore, IL10 developed a significant role in counteracting the LDL(-) inflammatory action.
OBJECTIVE: LDL(-) is a minor LDL subfraction that induces inflammatory factor release by endothelial cells. Since LDL(-) is present in plasma, its interaction with leucocytes, a cell type involved in atherosclerosis phenomena, is feasible; therefore, the aim of the current study was to evaluate LDL(-) effect on lymphocytes and monocytes isolated from human plasma. METHODS AND RESULTS: Mononuclear cells were incubated with LDL(+) and LDL(-) and expression and release of several inflammatory mediators were analyzed by protein membrane assay, ELISA and real-time RT-PCR. LDL(-) induced a significantly increased production versus LDL(+) in MCP1, GRObeta, GROgamma, IL6, IL8 and IL10 in monocytes as well as in lymphocytes. These induced molecules are inflammatory, except for IL10 which is considered an anti-inflammatory cytokine. Therefore, the role of IL10 was evaluated in experiments where exogenous IL10 or antibodies anti-IL10 or anti-IL10 receptor were added. IL10 addition diminished the release of the other factors induced by LDL(-) near to basal production both at protein and RNA level. In contrast, the antibody anti-IL10 increased inflammatory cytokine release around two-fold, whereas the antibody anti-IL10 receptor produced a lower effect. CONCLUSIONS: LDL(-) promoted inflammatory cytokine production in leucocytes; however, it also induced IL10 that minimized this effect. Therefore, IL10 developed a significant role in counteracting the LDL(-) inflammatory action.
Authors: Cristina Bancells; Sònia Benítez; Jordi Ordóñez-Llanos; Katariina Öörni; Petri T Kovanen; Ross W Milne; José L Sánchez-Quesada Journal: J Biol Chem Date: 2010-11-15 Impact factor: 5.157
Authors: Núria Puig; Lara Montolio; Pol Camps-Renom; Laia Navarra; Francesc Jiménez-Altayó; Elena Jiménez-Xarrié; Jose Luis Sánchez-Quesada; Sonia Benitez Journal: Cells Date: 2020-03-01 Impact factor: 6.600