With interest we noticed the article by Hayashi et al. in the May 15, 2009 issue of The Journal of Immunology (1). The authors reported the injection of Listeria into the ventricular system resulting in lethal “ventriculitis,” whereas injection into the brain parenchyma induced nonlethal meningoencephalitis. However, histopathology shows that Hayashi et al. induced brain abscess instead of meningoencephalitis by intraparenchymal injection (Fig. 2A of Ref. 1) and ventriculitis plus periventricular encephalitis by ventricular infection (Fig. 2F of Ref. 1), respectively.
The authors stress that their “encephalitis” model serves as a model for human cerebral listeriosis superior to the “ventriculitis” model claimed to be used by us. However, we (2, 3, 4) and others (5, 6, 7), whose pioneering work, unfortunately, escaped citation by Hayashi et al. (1), studied the course of disease upon injection of bacteria into the forebrain but not into the ventricular system. Under these conditions, ventriculitis starts in the fourth ventricle, which is far distant from the injection site (2). Thus, panels C–E in Fig. 1 of Ref. 1 , which appear to be intended to explain our model of cerebral listeriosis but surprisingly are not explained in Materials and Methods and Results (1), are incorrect.
Hayashi et al. also show that infection with 3 × 103 Listeria induces lethal cerebral listeriosis after injection into the brain parenchyma (Fig. 4A of Ref. 1), further refuting their conclusion that the anatomic site of infection is the major factor determining the course of cerebral listeriosis.
Hayashi et al. (1) question the use of recombinant and attenuated Listeria in experimental listeriosis. However, genetically manipulated Listeria are extremely helpful in analyzing the immunology and pathogenesis of systemic and cerebral listeriosis (8, 9, 10).
- Copyright © 2009 by The American Association of Immunologists, Inc.
References
- ↵
Hayashi, T., S. Nagai, H. Fujii, Y. Baba, E. Ikeda, T. Kawase, S. Koyasu. 2009. Critical roles of NK and CD8+ T cells in central nervous system listeriosis. J. Immunol. 182: 6360-6368.
- ↵
Schlüter, D., S. Chahoud, H. Lassmann, A. Schumann, H. Hof, M. Deckert-Schlüter. 1996. Intracerebral targets and immunomodulation of murine Listeria monocytogenes meningoencephalitis. J. Neuropathol. Exp. Neurol. 55: 14-24.
- ↵
Deckert, M., S. Virna, M. Sakowicz-Burkiewicz, S. Lütjen, S. Soltek, H. Bluethmann, D. Schlüter. 2007. Interleukin-1 receptor type 1 is essential for control of cerebral but not systemic listeriosis. Am. J. Pathol. 170: 990-1002.
- ↵
Schlüter, D., S. B. Oprisiu, S. Chahoud, D. Weiner, O. D. Wiestler, H. Hof, M. Deckert-Schlüter. 1995. Systemic immunization induces protective CD4+ and CD8+ T cell-mediated immune responses in murine Listeria monocytogenes meningoencephalitis. Eur. J. Immunol. 25: 2384-2391.
- ↵
Lechner, F., U. Sahrbacher, T. Suter, K. Frei, M. Brockhaus, U. Koedel, A. Fontana. 2000. Antibodies to the junctional adhesion molecule cause disruption of endothelial cells and do not prevent leukocyte influx into the meninges after viral or bacterial infection. J. Infect. Dis. 182: 978-982.
- ↵
Frei, K., D. Nadal, H. W. Pfister, A. Fontana. 1993. Listeria meningitis: identification of a cerebrospinal fluid inhibitor of macrophage listericidal function as interleukin 10. J. Exp. Med. 178: 1255-1261.
- ↵
Leist, T. P., K. Frei, S. Kam-Hansen, R. M. Zinkernagel, A. Fontana. 1988. Tumor necrosis factor α in cerebrospinal fluid during bacterial, but not viral, meningitis: evaluation in murine model infections and in patients. J. Exp. Med. 167: 1743-1748.
- ↵
Khanna, K. M., J. T. McNamara, L. Lefrançois. 2007. In situ imaging of the endogenous CD8 T cell response to infection. Science 318: 116-120.
- ↵
Brandl, K., G. Plitas, B. Schnabl, R. P. DeMatteo, E. G. Pamer. 2007. MyD88-mediated signals induce the bactericidal lectin RegIII γ and protect mice against intestinal Listeria monocytogenes infection. J. Exp. Med. 204: 1891-1900.
- ↵
Zehn, D., S. Y. Lee, M. J. Bevan. 2009. Complete but curtailed T-cell response to very low-affinity antigen. Nature 458: 211-214.
