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Acta Physiologica Congress

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Acta Physiologica 2011; Volume 201, Supplement 682
The 90th Annual Meeting of The German Physiological Society
3/26/2011-3/29/2011
Regensburg, Germany


ONTOGENETIC REGULATION OF HUMAN POLYMORPHONUCLEAR NEUTROPHIL RECRUITMENT
Abstract number: P206

*Nussbaum1 C., Gloning1 A., Pruenster1 M., Bierschenk1 S., Genzel-Boroviczeny2 O., Sperandio3 M.

Attenuation of the neonatal immune response contributes to the high rate of infection in newborns and particularly premature infants. While there is a growing understanding of innate immune functions in mature neonates, little is known about the ontogeny of neutrophil (PMN) recruitment. Here we studied the influence of gestational age on neutrophil and endothelial cell (EC) adhesive functions under flow.Using microflow chambers, we examined rolling and adhesion of neutrophils from premature and mature newborns. To investigate the adhesive properties of fetal endothelial cells (EC), we measured recruitment of adult neutrophils on LPS-treated HUVEC from premature and mature neonates. FACS analysis was performed to quantify the expression of adhesion molecules on neonatal PMN and EC. PMN rolling and adhesion correlated directly with gestational age and were almost absent in extremely premature infants. In addition, a marked reduction of PSGL-1 and Mac-1 expression on PMN was found. Interestingly, PMN from prematures also exhibited a significant reduction in rolling velocity. The adhesive properties of neonatal EC were equally dependent on gestational age with HUVEC from extreme prematures showing diminished E-selectin and ICAM-1 levels. Additional follow-up studies on extreme prematures provided evidence that maturation of PMN recruitment is not altered by extrauterine factors compared to intrauterine development. In summary, PMN recruitment in humans is ontogenetically regulated involving both neutrophil and endothelial cell function. In this context, the inability of very preterm neonates to sufficiently recruit PMN is likely to contribute to their increased susceptibility to life threatening infections.

To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 201, Supplement 682 :P206

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