The contribution of streptolysin O (SLO) from Streptococcus pyogenes to neutrophil infiltration in inflammatory lesions was determined by production of cytokine‐induced neutrophil chemoattractant (CINC)−1, −2 and −3, and macrophage inflammatory protein (MIP)‐1α by rat macrophages stimulated with SLO in culture. Active SLO induced the production of CINCs and MIP‐1α in dose‐ and time‐dependent manners. These inductions were ascertained by chemokine mRNA expression in macrophages. Streptolysin S was without effect. The SLO‐cholesterol complex induced the chemokine production in proportion to the residual hemolytic activity of the complex. In addition, the effects of SLO on the chemokine production were confirmed by the injection of active SLO into the preformed air pouch on the back of rats. The infiltration of neutrophils into the pouch fluid (exudate) increased steadily with a lag phase of about 2 hr. The major chemokine found in exudates was MIP‐1α but not CINCs. In this study, it became clear that active SLO, but not the inactive one, contributed to the production of MIP‐1α and CINCs in the conditioned medium and in exudates.

stiffness and pulse wave velocity / Aorta and carotid arteries 137 (0.94 to 1.01) p = 0.096; Obesity OR = 0.47 (0.29 to 1.77) p = 0.003 and Diabetes OR = 2.41 (1.15 -5.05) p = 0.020. Conclusions: According to the results obtained, genetic polymorphisms variables were not in the multivariate analysis equation to determine the increase of the PWV, which can be explained either by being included in the selected variables such as hypertension, or on the other hand, they may not have enough strength to remain in the equation. So, according to this study, PWV has much more to do with behaviors and traditional risk factors than the genetic heritage.P883 Endothelial dysfunction, pulse wave velocity and augmentation index are correlated in subjects with systemic arterial hypertension?