Interleukin-1 Receptor Type 1 Is Essential for Control of Cerebral but Not Systemic Listeriosis

Deckert, Martina; Virna, Simona; Sakowicz-Burkiewicz, Monika; Lütjen, Sonja; Soltek, Sabine; Bluethmann, Horst; Schlüter, Dirk

doi:10.2353/ajpath.2007.060507

Cited by 15 publications

(10 citation statements)

References 55 publications

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“…Therefore, TLR2-CD14 and additional, undefined pattern recognition receptors induce IL-1 and IL-18, which are required, together with IFN␥, IL-1, and TNF, to control L. monocytogenes infection. However, a recent report demonstrated that IL-1 signaling is dispensable for the control of systemic Listeria infection, but required to control cerebral listeriosis [37].…”

Section: Discussionmentioning

confidence: 99%

CD14 Works with Toll‐Like Receptor 2 to Contribute to Recognition and Control ofListeria monocytogenesInfection

Janot¹,

Sécher²,

Torres³

et al. 2008

J INFECT DIS

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Toll-like receptor 2 (TLR2) signaling has been shown to contribute to resistance to Listeria monocytogenes infection, as TLR2-deficient mice have a heightened susceptibility to infection with this organism. Because CD14 may associate with TLR2, we investigated the role of CD14 in Listeria responses. In both CD14-deficient and TLR2-deficient macrophages, nuclear factor kappaB translocation; CD40 and CD86; and the production of interleukin (IL)-12, IL-6, tumor necrosis factor, and nitric oxide are reduced. The absence of CD14 augmented susceptibility to Listeria infection, reduced survival, and diminished bacterial clearance, as observed in TLR2-deficient mice. Compared with C57BL/6 control mice, CD14-deficient mice were observed to have a greater number of hepatic microabscesses containing abundant neutrophils, these abscesses were larger in size, and there was reduced inducible nitric oxide synthase expression. Further, mice that are both CD14 deficient and TLR2 deficient display susceptibility to infection that is comparable to that of mice deficient in either CD14 or TLR2 alone. Therefore, the present data demonstrate the role of CD14 and TLR2 in the recognition and control of Listeria infection and host resistance.

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Section: Discussionmentioning

confidence: 99%

CD14 Works with Toll‐Like Receptor 2 to Contribute to Recognition and Control ofListeria monocytogenesInfection

Janot¹,

Sécher²,

Torres³

et al. 2008

J INFECT DIS

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“…For example, IL-1R is important for mice with a mixed 129/Sv × C57BL/6 background to control L. monocytogenes infection [22,23]. On the other hand, IL-1R deficiency does not affect the resistance of mice with a C57BL/6 background to systemic infection with L. monocytogenes, but increases the susceptibility to intracerebral infection [23,24]. Another study showed that IL-1β is dispensable for innate resistance to L. monocytogenes [25].…”

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confidence: 99%

The adaptor ASC exacerbates lethal Listeria monocytogenes infection by mediating IL‐18 production in an inflammasome‐dependent and ‐independent manner

et al. 2014

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Listeria monocytogenes induces the formation of inflammasomes and subsequent caspase-1 activation, and the adaptor apoptosis-associated speck-like protein containing a CARD (ASC) is crucial for this response. However, the role of ASC in L. monocytogenes infection in vivo is unclear. In this study, we demonstrate that ASC has a detrimental effect on host defense against L. monocytogenes infection at a lethal dose (10 6 CFU), but not at a sublethal dose (10 3 CFU). During lethal L. monocytogenes infection, serum levels of IL-18 and IL-10 were markedly elevated in WT mice, but not in ASC KO mice. IL-18 KO mice were more resistant to lethal L. monocytogenes infection than WT mice and had lower levels of serum IL-10. Furthermore, blockade of IL-10 receptor resulted in a reduction in bacterial counts, suggesting that ASC and IL-18 might exacerbate L. monocytogenes infection through induction of IL-10. We noticed that maturation of IL-18 during lethal infection was partially independent of caspase-1, but was critically dependent on ASC. ASC was required for the elevation of serum neutrophil serine protease activity, which correlated with caspase-1-independent IL-18 maturation and IL-10 production. Collectively, these results suggest that ASC plays a detrimental role in lethal L. monocytogenes infection through IL-18 production in an inflammasome-dependent and -independent manner.Keywords: ASC r Caspase-1 r IL-18 r Inflammasome r Listeria monocytogenes Additional supporting information may be found in the online version of this article at the publisher's web-site IntroductionListeria monocytogenes is a Gram-positive, intracellular parasitic bacterium, which causes foodborne listeriosis in humans Correspondence: Dr. Kohsuke Tsuchiya e-mail: tsuchiya.kohsuke.5w@kyoto-u.ac.jp [1,2]. Listeria monocytogenes invades and multiplies within the cytoplasm of various types of cells, including macrophages, epithelial cells, and hepatocytes [3,4]. Several virulence factors have been reported to support the intracellular parasitism of L. monocytogenes at various steps, including invasion of host cells, escape from endosomal compartments, evasion of autophagy, utilization of cytosolic nutrient sources, and cell-to-cell spread [3,4].C 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim www.eji-journal.eu Eur. J. Immunol. 2014. 44: 3696-3707 Innate immunity 3697Listeriolysin O, a 56 kDa protein encoded by the hly gene, is a member of the cholesterol-dependent cytolysin family and plays an essential role in the escape of L. monocytogenes from phagosomes, because mutant strains lacking the hly gene are avirulent and incapable of escaping from phagosomes and of multiplying in host phagocytes [3][4][5][6]. Inflammasomes are multiprotein complexes formed typically in the cytoplasm and serve as platforms for caspase-1 activation [7]. Each inflammasome consists of pro-caspase-1 and a receptor protein that belongs to the nucleotide-binding oligomerization domain like receptor (NLR) family or the HIN-200 family. Among NLR family, CARD domain cont...

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“…Histology and immunohistochemistry on frozen and paraffin sections were performed as described (18). To identify the OVA-expressing cells, double immunofluorescence staining was conducted on frozen sections.…”

Section: Histopathologymentioning

confidence: 99%

Molecular Mimicry between Neurons and an Intracerebral Pathogen Induces a CD8 T Cell-Mediated Autoimmune Disease

Sánchez‐Ruiz

Wilden

Müller

et al. 2008

The Journal of Immunology

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To identify basic mechanisms of how infections may induce a neuron-specific autoimmune response, we generated mice expressing OVA as neuronal autoantigen under control of the neuron-specific enolase promoter (NSE-OVA mice). Intracerebral, but not systemic, infection with attenuated Listeria monocytogenes-secreting OVA induced an atactic-paretic neurological syndrome in NSE-OVA mice after bacterial clearance from the brain, whereas wild-type mice remained healthy. Immunization with attenuated Listeria monocytogenes-secreting OVA before intracerebral infection strongly increased the number of intracerebral OVA-specific CD8 T cells aggravating neurological disease. T cell depletion and adoptive transfer experiments identified CD8 T cells as decisive mediators of the autoimmune disease. Importantly, NSE-OVA mice having received OVA-specific TCR transgenic CD8 T cells developed an accelerated, more severe, and extended neurological disease. Adoptively transferred pathogenic CD8 T cells specifically homed to OVA-expressing MHC class I+ neurons and, corresponding to the clinical symptoms, ∼30% of neurons in the anterior horn of the spinal cord became apoptotic. Thus, molecular mimicry between a pathogen and neurons can induce a CD8 T cell-mediated neurological disease, with its severity being influenced by the frequency of specific CD8 T cells, and its induction, but not its symptomatic phase, requiring the intracerebral presence of the pathogen.

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Interleukin-1 Receptor Type 1 Is Essential for Control of Cerebral but Not Systemic Listeriosis

Cited by 15 publications

References 55 publications

CD14 Works with Toll‐Like Receptor 2 to Contribute to Recognition and Control ofListeria monocytogenesInfection

CD14 Works with Toll‐Like Receptor 2 to Contribute to Recognition and Control ofListeria monocytogenesInfection

The adaptor ASC exacerbates lethal Listeria monocytogenes infection by mediating IL‐18 production in an inflammasome‐dependent and ‐independent manner

Molecular Mimicry between Neurons and an Intracerebral Pathogen Induces a CD8 T Cell-Mediated Autoimmune Disease

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