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J. Biol. Chem., Vol. 278, Issue 31, 28540-28546, August 1, 2003

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Processing of Seminal Plasma hCAP-18 to ALL-38 by Gastricsin

A NOVEL MECHANISM OF GENERATING ANTIMICROBIAL PEPTIDES IN VAGINA^*

Ole E. Sørensen  , Lone Gram ¶, Anders H. Johnsen ||, Emma Andersson **, Susanne Bangsbøll , G. Sandra Tjabringa , Pieter S. Hiemstra , Johan Malm **, Arne Egesten ** and Niels Borregaard 

From the Granulocyte Research Laboratory, the Department of Hematology, the ^||Department of Clinical Biochemistry, Fertility Clinic, Copenhagen University Hospital, Rigshospitalet, DK-2100 Copenhagen, Denmark, the ^¶Department of Seafood Research, Danish Institute for Fisheries Research, DK-2800 Lyngby, Denmark, the ^**Department of Laboratory Medicine, Malmö University Hospital, SE-205 02 Malmö, Sweden, and the Department of Pulmonology, Leiden University Medical Center, 2300 RC Leiden, The Netherlands

The human cathelicidin, hCAP-18, is expressed both in neutrophils and in epithelial cells. hCAP-18 is processed to the antimicrobial peptide LL-37 by proteinase 3 in neutrophils. hCAP-18 is highly expressed in the epididymis with a subsequent high concentration in seminal plasma where the protein is present in its unprocessed and antimicrobially inactive form. We report here that hCAP-18 in seminal plasma is processed to generate a 38-amino acid antimicrobial peptide ALL-38 by the prostate-derived protease gastricsin when incubated at a pH corresponding to the vaginal pH. In accordance with this, seminal plasma derived hCAP-18 was found in its processed form in the vagina following sexual intercourse. The antimicrobial activity of ALL-38 against a variety of microorganisms tested is equal to that of LL-37. This enzymatic activation of a proantimicrobial substance in seminal plasma following exposure to the vaginal milieu represents a novel mechanism to prevent infection following sexual intercourse.

Received for publication, February 14, 2003 , and in revised form, May 16, 2003.

^* This work was supported by grants from the Danish Medical Research Council, the A. P. Møller and Chastine Mærsk McKinney Møller Foundation, and the Copenhagen Hospital Corporation. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed: Host Defense Research Laboratory, Dept. of Medicine, David Geffen School of Medicine at UCLA, 10833 Le Conte Ave., 52-164 CHS, Los Angeles, CA 90095-1690. Tel.: 310-825-7499; Fax: 310-206-8766; E-mail: sorensen{at}ucla.edu.

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