Decreased systemic polymorphonuclear neutrophil (PMN) rolling without increased PMN adhesion in peritonitis at remote sites

Background: Previous in vitro studies have demonstrated that the host respo nse to intra-abdominal infection produces increased generalized polymorphon uclear neutrophil (PMN) adherence to vascular endothelial cells (ECs), whic h may lead to subsequent endothelial damage, leaky capillaries, and organ d ysfunction. There are scant data to demonstrate this enhanced systemic PMN adherence in vivo or the influence of PMN rolling on PMN endothelial adhere nce. Hypothesis: Systemic PMN adherence in the animal with sepsis is increased. Design: In vivo murine model of a 2-front infection using intravital micros copy of the cremasteric muscle to quantify PMN-EC adherence in a septic res ponse. Setting: Basic science laboratory and animal surgical facility. Patients or Other Participants: One hundred CD1 male mice. Interventions: Animals underwent cecal ligation and puncture peritonitis, c remasteric muscle Escherichia coli infection, both infections, or neither ( controls). Eighteen hours later, the mice underwent exteriorization of the cremasteric muscle under an intravital microscope for measurement of PMN-EC interactions. Blood was then drawn for calculation of circulating PMN coun ts. Main Outcome Measures: Adherence of PMNs, PMN rolling flux, PMN rolling vel ocity, and circulating PMN counts. Results: Circulatory mechanics did not differ between the groups. Unlike st atic in vitro systems, we could not detect an increase in PMN adherence aft er peritonitis with this dynamic in vivo model. A local (cremasteric) infec tion was associated with marked PMN adherence. Peritonitis was associated w ith reduced PMN adherence at a local infection site as well as reduced roll ing adhesion and PMN rolling velocity. Conclusions: The data suggest that intra-abdominal infection does not incre ase remote PMN adherence, and may actually result in reduction of systemic adherence via modulation of PMN rolling.