Innate immune protein C1q plays a dual role in the chronic inflammatory disease, atherosclerosis. Complement activation via C1q exacerbates pathology of atherosclerosis late in disease progression. However, early on C1q is protective, although its precise mechanism of action has not yet been elucidated. We hypothesize that complement- independent activities of C1q are involved in reprogramming macrophage responses. I examined the influence of C1q on macrophage inflammatory responses during clearance of oxLDL. Levels of pro-inflammatory cytokines IL-1β and IL-6 were down-regulated by C1q during macrophage clearance of oxLDL, whereas levels of the anti-inflammatory cytokine IL-10 are increased, measured via quantitative PCR and ELISA. An NFκB luciferase gene reporter assay suggested that C1q suppresses activation of NFκB during lipoprotein clearance in macrophages, which may provide one mechanism by which C1q down-regulates pro-inflammatory cytokine production. C1q-polarization of macrophages towards an anti-inflammatory (M2-like) phenotype may be important in dampening inflammation in early atherosclerosis.
|Advisor:||Fraser, Deborah A.|
|Commitee:||Lee-Fruman, Kay, Zhang, Mason|
|School:||California State University, Long Beach|
|School Location:||United States -- California|
|Source:||MAI 54/04M(E), Masters Abstracts International|
|Keywords:||C1q, Cytokine, Gene expression, Lipoprotein, Macrophage, Nf kappa b|
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