Intracerebral Targets and Immunomodulation of Murine Listeria monocytogenes Meningoencephalitis

Schlüter, Dirk; Chahoud, Soraya; Lassmann, H.; Schumann, Alexandra; H, Hof; Deckert-Schlüter, Martina

doi:10.1097/00005072-199601000-00002

Cited by 52 publications

(40 citation statements)

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“…Strong adhesion of L. monocytogenes to the choroid plexus was also observed in a mouse infection model (Schluter et al, 1996). Based on the observations reported here and elsewhere (Prats et al, 1992;Schluter et al, 1996), we propose a model for L. monocytogenes to breach the blood-brain barrier, causing . At least 20 plaques were randomly selected for each strain for determination of their relative sizes (diameter in arbitrary units; a.u.)…”

Section: Discussionsupporting

confidence: 82%

“…The entry of the bacterium into the epithelial cells of the choroid plexus is mediated by IspC via interaction with an unknown receptor; when within the epithelial cells, the bacterium undergoes cell-to-cell spread or enters into the CSF to undergo an extracellular phase prior to causing brain infection (encephalitis). Demonstration of the presence of L. monocytogenes in CSF (Brouwer et al, 2006, Schluter et al, 1996 supports the notion of L. monocytogenes undergoing an extracellular phase. Alternatively, L. monocytogenes could invade the microvascular endothelial cells through the interaction of InlB with a specific, as yet unidentified receptor, leading to encephalitis.…”

supporting

confidence: 57%

“…This suggests that when cultured human epithelial cells from the choroid plexus are not available, SCP cells are a good cell culture model for in vitro study of adhesion to and entry into the epithelial cells of the choroid plexus by L. monocytogenes, which has been shown to cause significant meningitis in sheep (Vandegraaff et al, 1981). Strong adhesion of L. monocytogenes to the choroid plexus was also observed in a mouse infection model (Schluter et al, 1996). Based on the observations reported here and elsewhere (Prats et al, 1992;Schluter et al, 1996), we propose a model for L. monocytogenes to breach the blood-brain barrier, causing .…”

Section: Discussionmentioning

confidence: 99%

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A novel cell wall-anchored peptidoglycan hydrolase (autolysin), IspC, essential for Listeria monocytogenes virulence: genetic and proteomic analysis

Wang

Lin

2008

Microbiology

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Section: Discussionsupporting

confidence: 82%

supporting

confidence: 57%

Section: Discussionmentioning

confidence: 99%

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A novel cell wall-anchored peptidoglycan hydrolase (autolysin), IspC, essential for Listeria monocytogenes virulence: genetic and proteomic analysis

Wang

Lin

2008

Microbiology

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“…Interestingly, these anatomic regions correspond to the predilection and entry sites of L. monocytogenes in cerebral listeriosis (19,20). Thus, intracerebral T cells were positioned optimally to prevent spread of Listeria to the brain and development of cerebral listeriosis.…”

Section: Discussionmentioning

confidence: 96%

Protective Immunosurveillance of the Central Nervous System by Listeria-Specific CD4 and CD8 T Cells in Systemic Listeriosis in the Absence of Intracerebral Listeria

Kwok

Miletić

Lütjen

et al. 2002

The Journal of Immunology

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The invasion of the CNS by pathogens poses a major risk for damage of the highly vulnerable brain. The aim of the present study was to analyze immunological mechanisms that may prevent spread of infections to the CNS. Intraperitoneal application of Listeria monocytogenes to mice induced infection of the spleen, whereas pathogens remained absent from the brain. Interestingly, Listeria-specific CD4 and CD8 T cells homed to the brain and persisted intracerebrally for at least 50 days after both primary and secondary infection. CD4 and CD8 T cells resided in the leptomeninges, in the choroid plexus, and, in low numbers, in the brain parenchyma. CD4 and CD8 T cells isolated from the brain early after infection (day 7) were characterized by an activated phenotype with spontaneous IFN-γ production, whereas at a later stage of infection (day 28) restimulation with Listeria-specific peptides was required for the induction of IFN-γ production by CD4 and CD8 T cells. In contrast to splenic T cells, T cells in the brain did not exhibit cytotoxic activity. Adoptively transferred T cells isolated from the brains of Listeria-infected mice reduced the bacterial load in cerebral listeriosis. The frequency of intracerebral Listeria-specific T cells was partially regulated by the time of exposure to Listeria and cross-regulated by CD4 and CD8 T cells. Collectively, these data reveal a novel T cell-mediated pathway of active immunosurveillance of the CNS during bacterial infections.

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“…inoculation of WT LM inevitably causes death of mice within 5 days before the onset of a LM-specific T cell response (27). The disease is characterized by a strong multiplication of LM in choroid plexus epithelial cells, ependymal cells, macrophages, microglia, and some neurons resulting in a prominent meningitis, ventriculitis, and encephalitis, and mice finally succumb to a necrotizing brain stem encephalitis (28). In addition, massive brain edema and neuronal apoptosis develop, which are reduced by intrathecally produced , and may be induced or aggravated by i.c.…”

Section: Isteria Monocytogenes (Lm)mentioning

confidence: 99%

TNF Is Important for Pathogen Control and Limits Brain Damage in Murine Cerebral Listeriosis

Virna¹,

Deckert

Lütjen³

et al. 2006

The Journal of Immunology

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Cerebral listeriosis is a life-threatening disease. However, little is known about the bacterial virulence factors responsible for the severe course of disease and the factors of the immune system contributing to the control of Listeria monocytogenes (LM) or even to the damage of the brain. To analyze the importance of the actA gene of LM, which mediates cell-to-cell spread of intracellular LM, the function of TNF in murine cerebral listeriosis was studied. C57BL/6 mice survived an intracerebral (i.c.) infection with actA-deficient LM, but succumbed to infection with wild-type (WT) LM. Upon infection with actA-deficient LM, macrophages and microglial cells rapidly, and later LM-specific CD4 and CD8 T cells, produced TNF. In contrast to WT mice, TNF-deficient animals succumbed to the infection within 4 days due to failure of control of LM. Histology identified a more severe meningoencephalitis, brain edema, and neuronal damage, but a reduced inducible NO synthase expression in TNF-deficient mice. Reciprocal bone marrow chimeras between WT and TNF-deficient mice revealed that hematogenously derived TNF was essential for survival, whereas TNF produced by brain-resident cells was less important. Death of TNF-deficient mice could be prevented by LM-specific T cells induced by an active immunization before i.c. infection. However, brain pathology and inflammation of immunized TNF-deficient mice were still more severe. In conclusion, these findings identify a crucial role of TNF for the i.c. control of LM and survival of cerebral listeriosis, whereas TNF was not responsible for the destruction of brain tissue.

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Intracerebral Targets and Immunomodulation of Murine Listeria monocytogenes Meningoencephalitis

Cited by 52 publications

References 0 publications

A novel cell wall-anchored peptidoglycan hydrolase (autolysin), IspC, essential for Listeria monocytogenes virulence: genetic and proteomic analysis

A novel cell wall-anchored peptidoglycan hydrolase (autolysin), IspC, essential for Listeria monocytogenes virulence: genetic and proteomic analysis

Protective Immunosurveillance of the Central Nervous System by Listeria-Specific CD4 and CD8 T Cells in Systemic Listeriosis in the Absence of Intracerebral Listeria

TNF Is Important for Pathogen Control and Limits Brain Damage in Murine Cerebral Listeriosis

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