RESUMO
Low back pain (LBP) affects 20 to 30% of the United States general population, making it the fifth most common reason for all physician visits in the U.S. The resultant financial burden on the U.S. health care industry continues to rise each year with recent estimates of over $80 billion spent annually. However, despite the dramatic rise in health care utilization and costs for this complaint, self-reported outcomes have not improved. The radiographic analysis of a healthy asymptomatic population vs. a cohort of LBP patients with lumbar degenerative disc disease, specifically as it relates to posture, spinal alignments, including lumbar lordosis, as well as other findings, may provide insight to more effectively care for the LBP patient and, in return, possibly help to rein in related health care costs.
RESUMO
Public interest in Echinacea is growing rapidly. Unfortunately, there is little scientific evidence to support claims of efficacy of this widely used botanical, and little information about potential mechanism of action. This study examines the ability of Echinacea to upregulate macrophage function and begins to elucidate the mechanism of Echinacea-induced macrophage activation. Murine peritoneal macrophages were cultured with E. purpurea extracts enriched for plant polysaccharide (EP). ELISA was used to measure cytokine production. MAPKs were blocked using specific inhibitors, and Western blotting used to identify phosphorylated proteins involved in signal transduction. To examine in vivo efficacy, EP was administered orally and Listeria monocytogenes given i.v. Mice were sacrificed three days post-infection to determine bacterial load in the spleen. We demonstrate that an endotoxin-free EP extract activates the innate immune response, stimulating production of IL-6, TNF, IL-12, and NO from macrophages in vitro. Along with evidence of enhanced macrophage function, we found that oral EP reduces bacterial burden during infection by Listeria monocytogenes, demonstrating its efficacy in vivo. EP initiates a signaling cascade within macrophages through both TLR4-dependent and -independent mechanisms, involving ERK, p38 and JNK, and ultimately the activation of NF-kappaB.
