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Infection and Immunity, February 2001, p. 1093-1100, Vol. 69, No. 2
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.2.1093-1100.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Neural Route of Cerebral Listeria monocytogenes Murine Infection: Role of Immune Response Mechanisms in Controling Bacterial Neuroinvasion

Yuxuan Jin,1,* Lone Dons,2 Krister Kristensson,1 and Martín E. Rottenberg3,*

Department of Neuroscience1 and Microbiology and Tumor Biology Center,3 Karolinska Institutet, Stockholm, Sweden, and Department of Veterinary Microbiology, The Royal Veterinary and Agricultural University, Fredriksberg, Denmark2

Received 19 July 2000/Returned for modification 22 August 2000/Accepted 25 September 2000

The pathologic features of cerebral Listeria monocytogenes infection strongly suggest that besides hematogenous spread, bacteria might also spread via a neural route. We propose that after snout infection of recombination activating gene 1 (RAG-1)-deficient mice, L. monocytogenes spreads to the brain via a neural route. The neural route of invasion is suggested by (i) the immunostaining of L. monocytogenes in the trigeminal ganglia (TG) and brain stem but not in other areas of the brain; (ii) the kinetics of bacterial loads in snout, TG, and brain; and (iii) the increased resistance of mice infected with a plcB bacterial mutant (unable to spread from cell to cell). Gamma interferon (IFN-gamma ) plays a protective role in neuroinvasion; inducible nitric oxide synthase (iNOS) accounts only partially for the protection, as shown by a comparison of the susceptibilities of IFN-gamma receptor (IFN-gamma R)-deficient, iNOS-deficient, and wild-type mice to snout infection with L. monocytogenes. The dramatically enhanced susceptibility of RAG-1-deficient, IFN-gamma R gene-deficient mice indicated the overall importance of innate immune cells in the release of protective levels of IFN-gamma . The source of IFN-gamma appeared to be NK cells, as shown by use of RAG-1-deficient, gamma -chain receptor gene-deficient mice; NK cells played a relevant protective role in neuroinvasion through a perforin-independent mechanism. In vitro evidence indicated that IFN-gamma can directly induce bacteriostatic mechanisms in neural tissue.

* Corresponding author. Mailing address: Microbiology and Tumor Biology Center, Karolinska Institute, Nobelsvägen 16, S 171 77 Stockholm, Sweden. Phone: 46-8-728-6232. Fax: 46-8-32-8878. E-mail: Martin.Rottenberg{at}mtc.ki.se.

Infection and Immunity, February 2001, p. 1093-1100, Vol. 69, No. 2
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.2.1093-1100.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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