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Infection and Immunity, December 2006, p. 6982-6991, Vol. 74, No. 12
0019-9567/06/$08.00+0     doi:10.1128/IAI.01043-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Induction of the Antimicrobial Peptide CRAMP in the Blood-Brain Barrier and Meninges after Meningococcal Infection{triangledown}

Peter Bergman,1 Linda Johansson,2 Hong Wan,3 Allison Jones,3 Richard L. Gallo,4 Gudmundur H. Gudmundsson,5 Tomas Hökfelt,6 Ann-Beth Jonsson,3 and Birgitta Agerberth1*

Department of Medical Biochemistry and Biophysics, Karolinska Institutet, SE-171 77 Stockholm, Sweden,1 Center for Infectious Medicine, Department of Medicine, Karolinska University Hospital Huddinge, SE-141 86 Stockholm, Sweden,2 Department of Medical Biochemistry and Microbiology, Box 582, Biomedical Center, Uppsala University, SE-751 23 Uppsala, Sweden,3 Division of Dermatology, University of California, and Veterans Affairs San Diego Healthcare Center, San Diego, California 92161,4 Institute of Biology, University of Iceland, Reykjavik, Iceland,5 Department of Neuroscience, Karolinska Institutet, SE-171 77 Stockholm, Sweden6

Received 4 July 2006/ Returned for modification 23 August 2006/ Accepted 28 September 2006

Antimicrobial peptides are present in most living species and constitute important effector molecules of innate immunity. Recently, we and others have detected antimicrobial peptides in the brain. This is an organ that is rarely infected, which has mainly been ascribed to the protective functions of the blood-brain barrier (BBB) and meninges. Since the bactericidal properties of the BBB and meninges are not known, we hypothesized that antimicrobial peptides could play a role in these barriers. We addressed this hypothesis by infecting mice with the neuropathogenic bacterium Neisseria meningitidis. Brains were analyzed for expression of the antimicrobial peptide CRAMP by immunohistochemistry in combination with confocal microscopy. After infection, we observed induction of CRAMP in endothelial cells of the BBB and in cells of the meninges. To explore the functional role of CRAMP in meningococcal disease, we infected mice deficient of the CRAMP gene. Even though CRAMP did not appear to protect the brain from invasion of meningococci, CRAMP knockout mice were more susceptible to meningococcal infection than wild-type mice and exhibited increased meningococcal growth in blood, liver, and spleen. Moreover, we could demonstrate that carbonate, a compound that accumulates in the circulation during metabolic acidosis, makes meningococci more susceptible to CRAMP.

* Corresponding author. Mailing address: Department of Medical Biochemistry and Biophysics, Scheeles vag 2, Karolinska Institutet, SE-171 77 Stockholm, Sweden. Phone: 46 85 24 87 781. Fax: 46 833 7462. E-mail: birgitta.agerberth{at}ki.se.

{triangledown} Published ahead of print on 9 October 2006.

Editor: J. N. Weiser

Infection and Immunity, December 2006, p. 6982-6991, Vol. 74, No. 12
0019-9567/06/$08.00+0     doi:10.1128/IAI.01043-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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