Fig. 4.
Effect of cardiomyocyte- and myeloid-specific MyD88 deletion on cytokine production in plasma at 6 h (A) and 18 h (B) after lipopolysaccharide (LPS) administration. Cardiac- (α-MHC-MyD88−/−), myeloid- (Lyz-MyD88−/−) MyD88 deletion mice, control (MyD88fl/fl) mice, and systemic MyD88 knockout (MyD88−/−) mice were treated with LPS (15 mg/kg, intraperitoneal injection) or saline. Six or 18 h later, blood was collected. Plasma interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNFα) were measured with a multiplex fluorescent bead-based immunoassay. Each error bar represents mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, n = 3 mice in MyD88−/− Saline group, n = 4 mice in other Saline groups and MyD88−/− LPS group, n = 7 mice in other LPS groups. Lyz-MyD88−/− = myeloid-specific MyD88 knockout mice; α-MHC = α-myosin heavy chain; α-MHC-MyD88−/− = cardiomyocyte-specific MyD88 knockout mice; MyD88 = myeloid differentiation factor 88; MyD88−/− = MyD88 knockout mice; MyD88fl/fl = MyD88-loxP control mice.

Effect of cardiomyocyte- and myeloid-specific MyD88 deletion on cytokine production in plasma at 6 h (A) and 18 h (B) after lipopolysaccharide (LPS) administration. Cardiac- (α-MHC-MyD88−/−), myeloid- (Lyz-MyD88−/−) MyD88 deletion mice, control (MyD88fl/fl) mice, and systemic MyD88 knockout (MyD88−/−) mice were treated with LPS (15 mg/kg, intraperitoneal injection) or saline. Six or 18 h later, blood was collected. Plasma interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNFα) were measured with a multiplex fluorescent bead-based immunoassay. Each error bar represents mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, n = 3 mice in MyD88−/− Saline group, n = 4 mice in other Saline groups and MyD88−/− LPS group, n = 7 mice in other LPS groups. Lyz-MyD88−/− = myeloid-specific MyD88 knockout mice; α-MHC = α-myosin heavy chain; α-MHC-MyD88−/− = cardiomyocyte-specific MyD88 knockout mice; MyD88 = myeloid differentiation factor 88; MyD88−/− = MyD88 knockout mice; MyD88fl/fl = MyD88-loxP control mice.

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