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Department of Laboratory Medicine, Division of Microbiology, Immunology and Glycobiology (MIG), Lund University, Lund, Sweden, and The Wright Flemming Institute, Imperial College School of Medicine, London, England
Correspondence: Catharina Svanborg, Department of Laboratory Medicine, Division of MIG, Lund University, Sölvegatan 23, 223 62 Lund, Sweden. E-mail: catharina.svanborg{at}mig.lu.se
Neutrophil migration to infected mucosal sites involves a series of complex interactions with molecules in the lamina propria and at the epithelial barrier. Much attention has focussed on the vascular compartment and endothelial cells, but less is known about the molecular determinants of neutrophil behavior in the periphery. We have studied urinary tract infections (UTIs) to determine the events that initiate neutrophil recruitment and interactions of the recruited neutrophils with the mucosal barrier. Bacteria activate a chemokine response in uroepithelial cells, and the chemokine repertoire depends on the bacterial virulence factors and on the specific signaling pathways that they activate. In addition, epithelial chemokine receptor expression is enhanced. Interleukin (IL)-8 and CXCR1 direct neutrophil migration across the epithelial barrier into the lumen. Indeed, mIL-8Rh knockout mice showed impaired transepithelial neutrophil migration, with tissue accumulation of neutrophils, and these mice developed renal scarring. They had a defective antibacterial defense and developed acute pyelonephritis with bacteremia. Low CXCR1 expression was also detected in children with acute pyelonephritis. These results demonstrate that chemokines and chemokine receptors are essential to orchestrate a functional antimicrobial defense of the urinary tract mucosa. Mutational inactivation of the IL-8R caused both acute disease and chronic tissue damage.
Key Words: urinary tract infection • bacterial virulence factors • neutrophil migration • innate immunity • chemokines
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