Rat RANTES (Luminometer) ELISA Kit

Inflammation and immunity are central in the pathobiology of pulmonary vascular disorders. Preliminary headway has been made in understanding the relationships between inflammatory proteins and clinical parameters in pediatric congenital heart disease. In this study, we analyzed serum levels of macrophage migration inhibitory factor (MIF) and regulated on activation normal T cell expressed and secreted chemokine (RANTES) in 87 patients with unrestrictive congenital cardiac communications and signs of pulmonary hypertension (age 2-36 months) and 50 pediatric controls. They were investigated in relation to clinical and hemodynamic parameters and the presence of Down syndrome. Hemodynamics was assessed by transthoracic Doppler echocardiography and cardiac catheterization. Chemokines were analyzed in serum using a chemiluminescence assay. The highest MIF levels were observed in very young subjects with heightened pulmonary vascular resistance but who presented a positive response to vasodilator challenge with inhaled nitric oxide. In contrast, RANTES levels were higher in patients with pulmonary overcirculation and congestion, correlating nonlinearly with pulmonary blood flow. Levels of both chemokines were higher in subjects with Down syndrome than in nonsyndromic individuals, but the difference was observed only in patients, not in the control group. In patients with Down syndrome, there was a direct relationship between preoperative serum MIF and the level of pulmonary artery pressure observed 6 months after surgical repair of cardiac anomalies. Thus, it was interesting to observe that MIF, which is key in the innate immune response and chemokine RANTES, which is highly expressed in respiratory viral infections were related to clinical and hemodynamic abnormalities associated with pediatric congenital heart disease.

Objective Myeloid-related protein-14 (MRP14) and its binding partner MRP8 play an essential role in innate immune function and have been implicated in a variety of inflammatory diseases. However, the role of MRP14 in obesity-induced inflammation and insulin resistance is not well defined. This study investigated the role of MRP14 in macrophage-mediated adipose tissue inflammation and obesity-induced insulin resistance. Subjects and results Wild-type (WT) and Mrp14(-/-) mice were fed with a high-fat diet or normal chow for 12 weeks. Tissue-resident macrophages in both adipose tissue and liver from obese WT mice expressed higher levels of MRP14 in the visceral adipose fat and liver compared with the lean mice. Mrp14(-/-) mice demonstrated a significantly improved postprandial insulin sensitivity, as measured by intraperitoneal glucose tolerance test and insulin tolerance testing. Macrophages secreted MRP14 in response to inflammatory stimuli, such as LPS. Extracellular MRP8/14 induced the production of CCL5 and CXCL9. Deficiency of MRP14 did not affect macrophage proliferation, mitochondrial respiration, and glycolytic function, but Mrp14(-/-) macrophages showed a reduced ability to attract T cells. Depletion of the extracellular MRP14 reduced the T cell attracting ability of WT macrophages to a level similar to Mrp14(-/-) macrophages. Conclusion Our data indicate that MRP14 deficiency decreases obesity-induced insulin resistance and MRP8/14 regulates T-cell recruitment through the induction of T-cell chemoattractant production from macrophages.