Expression data of C.pn treated foam cell

C.pn potentiated hyperlipidemia-induced inflammasome activity in cultured macrophages and in foam cells in atherosclerotic lesions of Ldlr–/– mice. We discovered that C.pn-induced extracellular IL-1β triggers a negative feedback loop to inhibit GPR109a and ABCA1 expression and cholesterol efflux leading to accumulation of intracellular cholesterol and foam cell formation. Gpr109a and Abca1 were both upregulated in plaque lesions in Nlrp3–/– mice in both hyperlipidemic and C.pn infection models. We sued microarrays to detail the gene expression underlying C.pn and ox-LDL treatment on mice periteneal macrophages to study the regulating of ABCA1 related genes with NLRP3 manutation WT and NLRP3 KO periteneal macrophage were treated for RNA extraction and hybridization on Affymetrix microarrays. Four-condition experiment using peritoneal macrophages: WT PBS; WT [Cpn + oxLDL ] 8h; NLRP3 KO PBS;NLRP3 KO [Cpn + oxLDL] 8h to analyze the expression profiles.