In sepsis, α3β1-integrin expression is upregulated on hyperinflammatory neutrophils and promotes their recruitment to affected sites through interactions with extracellular matrix proteins, such as laminin. Neutrophil infiltration may result in hyperinflammation, tissue damage, and organ failure. Inhibition of α3β1 integrin blocks neutrophil extravasation; neutrophils are entrapped between the endothelium and the pericytes. Inhibition of α3β1 integrin could thereby prevent hyperinflammation and promote survival in sepsis.