Integrin subunits alphav and beta3 form a dimer, alphavbeta3, which is expressed on normal neutrophils and endothelium. We investigated the expression of integrin subunits alphav and beta3 in acute lung inflammation in Sprague-Dawley rats ( n=5 each) following intratracheal challenge with Escherichia coli or Streptococcus pneumoniae, which induce neutrophil recruitment through different mechanisms. Control rats ( n=5) were given endotoxin-free saline. Both bacterial challenges induced similar levels of recruitment of neutrophils in lungs. Western blots showed lower expression of integrin subunits alphav and beta3 in lungs challenged with E. coli compared to those given S. pneumoniae. Immunohistochemistry and immunogold electron microscopy localized both integrin subunits in neutrophils and endothelium in the control and treated rat lungs. Quantitative immunohistochemistry showed that E. coli-challenged rat lungs contained a lower percentage of neutrophils expressing integrin subunits alphav and beta3 compared to those challenged with S. pneumoniae ( P<0.05). We conclude that E. coli infection decreased the percentage of neutrophils expressing integrin subunits alphav and beta3 compared to S. pneumoniae infection. These data lay the foundation for further characterization of these integrin subunits in neutrophil migration specifically in S. pneumoniae infection that utilizes molecules other than beta2 integrins for neutrophil recruitment.