Accumulation of T cells and macrophages in athero-sclerotic plaques and the formation of antibodies directed against plaque proteins suggests that adaptive immunity contributes to the development of atherosclerosis. The contribution of Th1 and Th2 helper cell subsets to atherogenesis was studied in a murine model by interbreeding apolipoprotein E-deficient (apoE
mice with mice deficient in key cytokines that drive either Th1 responses [interleukin (IL)-12] or Th2 responses (IL-4). Compared to apoE؊/؊ mice, apoE ؊/؊ /IL-12 ؊/؊ mice had a 52% reduction in plaque area in the aortic root at 30 weeks of age (P < 0.001). ApoE ؊/؊ /IL-4 ؊/؊ mice had a 27% reduction in plaque area compared to apoE ؊/؊ mice (P < 0.05) at 30 weeks of age, but their plaques were significantly larger than in apoE ؊/؊ /IL-12 ؊/؊ mice at this stage (P < 0.05). By 45 weeks of age, there were no significant differences in lesion sizes in the aortic root between the strains, however apoE ؊/؊ /IL-4 ؊/؊ mice showed a 58% and 64% decrease in disease in their aortic arch compared to apoE ؊/؊ (P < 0.05) and apoE ؊/؊ /IL-12 ؊/؊ (P < 0.05) mice, respectively, and a 78% decrease in thoracic lesions compared to apoE ؊/؊
Early use of CVVH at 2 L/hr did not reduce the circulating concentrations of several cytokines and anaphylatoxins associated with septic shock, or the organ dysfunction that followed severe sepsis. CVVH using current technology cannot be recommended as an adjunct to the treatment of septic shock unless severe acute renal failure is present.
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