P-Selectin/ICAM-1 double mutant mice: Acute emigration of neutrophils into the peritoneum is completely absent but is normal into pulmonary alveoli.

Bullard DC, Qin L, Lorenzo I, Quinlin WM, Doyle NA, Bosse R, Vestweber D, Doerschuk CM, Beaudet AL:
P-Selectin/ICAM-1 double mutant mice: Acute emigration of neutrophils into the peritoneum is completely absent but is normal into pulmonary alveoli.
Journal of Clinical Investigation 1995 April;95:1782-1788

ABSTRACT
Neutrophil emigration during an inflammatory response is mediated through interaction between adhesion molecule on endothelial cells and neutrophils. P-Selectin mediates rolling or slowing of neutrophils, while intercellular adhesion molecule-1 (ICAM-1) contributes to the firm adhesion and emigration of neutrophils. Removing the function of either molecule partially prevents neutrophil emigraion. To analyze further the role of P-selectin and ICAM-1, we we have generated a line of mice with mutation in both of these molecules. While mice with either mutation alone show a 60-70% reduction in acute neutrophil emigration into the peritoneum during Streptococus pneumoniae-induced peritonitis, double mutant mice show a complete loss of neutrophil emigration. In contrast, neutrophil emigration into the alveolar spaces during acute S. pneumoniae-induced pneumonia is normal in double mutant mice. These data demonstrate organ-specific differences, since emigration inot the pertoneum requires both adhesion molecules while emigration into the lung requires neither. In the peritoneum, P-selectin-independent and ICAM-1-independent adhesive mechanisms permit reduced emigration when one of these molecules is deficient, but P-selectin-independent mechanisms cannot lead to ICAM-1-independent firm adhesion and emigration.