Nature Medicine
- 12, 636 - 641 (2006)
Published online: 4 June 2006; | doi:10.1038/nm1407
The antimicrobial peptide cathelicidin protects the urinary tract against invasive bacterial infectionMilan Chromek1, Zuzana Slamová1, Peter Bergman2, László Kovács3, L'udmila Podracká4, Ingrid Ehrén5, Tomas Hökfelt6, Gudmundur H Gudmundsson7, Richard L Gallo8, Birgitta Agerberth2 & Annelie Brauner11
Department of Clinical Microbiology, Microbiology and Tumorbiology Center, Karolinska University Hospital and Karolinska Institutet, SE-171 76 Stockholm, Sweden. 2
Department of Medical Biochemistry and Biophysics, Karolinska Institutet, SE-171 77 Stockholm, Sweden. 3
Department of Pediatrics, Comenius University School of Medicine, 833 40 Bratislava, Slovakia. 4
Department of Pediatrics, Pavol Jozef  afárik University School of Medicine, 040 66 Ko ice, Slovakia. 5
Department of Urology, Karolinska University Hospital Solna, SE-171 76 Stockholm, Sweden. 6
Department of Neuroscience, Karolinska Institutet, SE-171 77 Stockholm, Sweden. 7
Biology Institute, University of Iceland, 101 Reykjavik, Iceland. 8
Division of Dermatology, University of California, San Diego, California 92161, USA.
Correspondence should be addressed to Annelie Brauner Annelie.Brauner@ki.se The urinary tract functions in close proximity to the outside environment, yet must remain free of microbial colonization to avoid disease. The mechanisms for establishing an antimicrobial barrier in this area are not completely understood. Here, we describe the production and function of the cathelicidin antimicrobial peptides LL-37, its precursor hCAP-18 and its ortholog CRAMP in epithelial cells of human and mouse urinary tract, respectively. Bacterial contact with epithelial cells resulted in rapid production and secretion of the respective peptides, and in humans LL-37/hCAP-18 was released into urine. Epithelium-derived cathelicidin substantially contributed to the protection of the urinary tract against infection, as shown using CRAMP-deficient and neutrophil-depleted mice. In addition, clinical E. coli strains that were more resistant to LL-37 caused more severe urinary tract infections than did susceptible strains. Thus, cathelicidin seems to be a key factor in mucosal immunity of the urinary tract.
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