Production of IL-12 and IL-18 in human dendritic cells upon infection by<i>Listeria monocytogenes</i>

Kolb‐Mäurer, Annette; Kämmerer, Ulrike; Mäurer, Mathias; Gentschev, Ivaylo; Bröcker, Eva B.; Rieckmann, Peter; Kämpgen, Eckhart

doi:10.1016/s0928-8244(02)00470-4

Cited by 34 publications

(14 citation statements)

References 36 publications

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“…LTA also induces less IL-12 than LPS and subsequently IFN-␥ (64,91). The cytokine pattern produced by LTA is similar to that induced by the whole bacterium (200,210).…”

Section: Staphylococcal Structures Recognized By Tlr2mentioning

confidence: 69%

Recognition ofStaphylococcus aureusby the Innate Immune System

2005

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The gram-positive bacterium Staphylococcus aureus is a major pathogen responsible for a variety of diseases ranging from minor skin infections to life-threatening conditions such as sepsis. Cell wall-associated and secreted proteins (e.g., protein A, hemolysins, and phenol-soluble modulin) and cell wall components (e.g., peptidoglycan and alanylated lipoteichoic acid) have been shown to be inflammatory, and these staphylococcal components may contribute to sepsis. On the host side, many host factors have been implicated in the innate detection of staphylococcal components. One class of pattern recognition molecules, Toll-like receptor 2, has been shown to function as the transmembrane component involved in the detection of staphylococcal lipoteichoic acid and phenol-soluble modulin and is involved in the synthesis of inflammatory cytokines by monocytes/macrophages in response to these components. Nod2 (nucleotide-binding oligomerization domain 2) is the intracellular sensor for muramyl dipeptide, the minimal bioactive structure of peptidoglycan, and it may contribute to the innate immune defense against S. aureus. The staphylococcal virulence factor protein A was recently shown to interact directly with tumor necrosis factor receptor 1 in airway epithelium and to reproduce the effects of tumor necrosis factor alpha. Finally, peptidoglycan recognition protein L is an amidase that inactivates the proinflammatory activities of peptidoglycan. However, peptidoglycan recognition protein L probably plays a minor role in the innate immune response to S. aureus. Thus, several innate immunity receptors may be implicated in host defense against S. aureus

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“…LTA also induces less IL-12 than LPS and subsequently IFN-␥ (64,91). The cytokine pattern produced by LTA is similar to that induced by the whole bacterium (200,210).…”

Section: Staphylococcal Structures Recognized By Tlr2mentioning

confidence: 69%

Recognition ofStaphylococcus aureusby the Innate Immune System

2005

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“…This potential role of GM-CSF, in combination with other cytokines, for increasing the antibacterial competence of macrophages has already been advocated [22]. More specifically, GM-CSF could also cooperate for defense against Listeria infection with other proinflammatory cytokines, such as interleukin (IL)-12 [31,32] and IL-18 [33,34]. Intriguingly, the administration of a traditional Chinese medicine that protects against Listeria infection in mice has been shown to trigger the production of IL-1, IL-6, and GM-CSF [35].…”

Section: Discussionmentioning

confidence: 99%

Impairment of Growth ofListeria monocytogenesin THP‐1 Macrophages by Granulocyte Macrophage Colony‐Stimulating Factor: Release of Tumor Necrosis Factor–α and Nitric Oxide

et al. 2004

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Background. Listeria monocytogenes tends to survive in phagocytes. Granulocyte macrophage colony-stimulating factor (GM-CSF) protects mice against L. monocytogenes infection, and mice knocked out for the GM-CSF gene are more susceptible to these infections.Methods. THP-1 cells were used to characterize the GM-CSF receptor (binding isotherms; STAT5 phosphorylation), measure the intracellular growth of L. monocytogenes (5 h after phagocytosis), examine the influence of a 24-h incubation with GM-CSF before infection, measure the production of tumor necrosis factor (TNF)-a and the expression of nitric oxide synthase (iNOS), and evaluate the influence of anti-GM-CSF receptor (GMCSFRa) and anti-TNF-a antibodies and the addition of N q -nitro-L-arginine methyl ester (L-NAME) and catalase.Results. THP-1 cells display functional GM-CSFRa. GM-CSF impairs the intracellular growth of L. monocytogenes to ∼65% of its value in unstimulated cells. This effect is abolished by anti-GM-CSFRa, anti-TNF-a antibodies, and catalase (and, to a lesser extent, by L-NAME). GM-CSF stimulates the release of TNF-a and the expression of iNOS. TNF-a added to unstimulated cells (even in large amounts) does not fully reproduce the impairment in the growth of L. monocytogenes caused by GM-CSF.Conclusions. GM-CSF impairs the intracellular growth of L. monocytogenes by a synergistic action of the GM-CSF-triggered release of autocrine TNF-a and hydrogen peroxide and the production of NO (associated with the stimulation of the expression of iNOS).

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“…Nevertheless, in a recent study in BALB/c mice, the cytokine gene expression of gastric tissue was functionally not impaired after L. monocytogenes infection (Park et al 2004). For IL-12 and IL-18, produced by L. monocytogenes-infected human DC (see: Kolb-Ma¨urer et al 2003a), gene expression was not reduced in the infected animals; on the contrary, it displayed a parallel increase with progressing (Park et al 2004), which might indicate a similar active synthesis in the mouse DC also.…”

Section: Discussionmentioning

confidence: 86%

“…Human DC are known to phagocytose L. monocytogenes and to subsequently mature (Paschen et al 2000;Kolb-Ma¨urer et al 2000, 2003a. It has been found that opsonization of L. monocytogenes with human serum significantly enhances phagocytosis of the DC via FccRIII (CD16)-mediated receptor uptake.…”

Section: Introductionmentioning

confidence: 99%

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Human dendritic cells process and present Listeria antigens for in vitro priming of autologous CD4+ T lymphocytes

Eppler

Walch

Latinovic-Golic

et al. 2005

Histochem Cell Biol

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The role of human dendritic cells (DC) in the immune response toward intracellularly growing Listeria was analyzed under in vitro conditions using several morphological and functional methods. DC incubated with Listeria innocua and L. monocytogenes, respectively, readily phagocytosed the bacteria. Listeria did not impair viability and immunogenic potential of human DC. Listerial antigens were found to be processed within the lysosomal compartment of DC and colocalized with major histocompatibility complex (MHC) class II molecules, as shown by fluorescence and transmission electron microscopy. DC challenged with apathogenic L. innocua were highly effective in priming autologous naı¨ve T cells (mainly CD4+) in vitro. The T cells strongly proliferated in the presence of DC incubated with L. innocua, which could be significantly inhibited by anti-MHC II mAb. L. innocua-primed T cells were also successfully stimulated by DC harboring the pathogenic L. monocytogenes, either the wild-type strain EGD or the p60 reduced mutant strain RIII. From our results, we conclude that human DC infected with nonpathogenic intracellular bacteria are able to efficiently prime naı¨ve T cells, which are then suitable for recognition of antigens derived from related virulent bacterial species. This in vitro human model provides an interesting tool for basic research in infectious immunology and possibly for a new immunotherapy.

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Production of IL-12 and IL-18 in human dendritic cells upon infection byListeria monocytogenes

Cited by 34 publications

References 36 publications

Recognition ofStaphylococcus aureusby the Innate Immune System

Recognition ofStaphylococcus aureusby the Innate Immune System

Impairment of Growth ofListeria monocytogenesin THP‐1 Macrophages by Granulocyte Macrophage Colony‐Stimulating Factor: Release of Tumor Necrosis Factor–α and Nitric Oxide

Human dendritic cells process and present Listeria antigens for in vitro priming of autologous CD4+ T lymphocytes

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