Rapid neutrophil recruitment is critical for the efficient clearance of bacterial pathogens from the lungs. Although β2 integrins and their activation are required for neutrophil recruitment from postcapillary venules of the systemic circulation into inflamed tissues, the involvement of integrins in neutrophil recruitment in response to respiratory infection varies among bacterial pathogens. For stimuli eliciting β2 integrin-dependent neutrophil influx, including Pseudomonas aeruginosa, it remains unclear whether the activation of β2 integrins is an essential step in this process. In the current study, we analyze neutrophil trafficking within the lungs of mice infected with Pseudomonas aeruginosa and evaluate the role of β2 integrin activation through genetic deletion of talin-1 or Kindlin-3 or by pharmacological inhibition of high-affinity β2 integrins using a small molecule allosteric antagonist. We observe that attenuation of high-affinity β2 integrins leads to an enhancement of neutrophil emigration into lung interstitium and airspaces. Neutrophil effector functions, including the production of reactive oxygen species and the phagocytosis of bacteria, are only partially dependent on high-affinity β2 integrins. These results reveal a mechanism by which activated β2 integrins limit neutrophil entry into the lung tissue and airspaces during acute pseudomonal pneumonia and suggest potential strategies for modulating neutrophil-mediated host defense.