Production of Interferon‐α/β by Murine Dendritic Cell Lines Stimulated by Virus and Bacteria

Eloranta, Maija‐Leena; Sandberg, Kristian; Ricciardi‐Castagnoli, Paola; Lindahl, Mattias; Alm, G.

doi:10.1046/j.1365-3083.1997.d01-120.x

Cited by 40 publications

(26 citation statements)

References 32 publications

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“…It is therefore conceivable that this process may also directly or indirectly contribute to the peripheral activation of neutrophils and potentially the patient gene expression signature observed in this study. Indeed, infectious bacteria (e.g., Chlamydia, S. aureus, E. coli) have previously been reported to increase IFN-␣ levels (50,51). Comparison of our results with published data for neutrophils stimulated with LPS indicates similarities in gene expression datasets with respect to ISG (52).…”

Section: Discussionsupporting

confidence: 74%

Periodontitis Associates with a Type 1 IFN Signature in Peripheral Blood Neutrophils

Wright

Matthews

Chapple

et al. 2008

The Journal of Immunology

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Peripheral blood neutrophils from periodontitis patients exhibit a hyperreactive and hyperactive phenotype (collectively termed hyperresponsivity) in terms of production of reactive oxygen species (ROS). The molecular basis for this phenomenon, however, has yet to be determined. Our objectives were to identify genes differentially expressed in hyperresponsive peripheral blood neutrophils from chronic periodontitis patients relative to periodontally healthy controls and use these data to identify potential contributory pathways to the hyperresponsive neutrophil phenotype. Using microarray technology we demonstrated differential expression of 163 genes (149 increased, 14 decreased) representing a range of ontological classes. There was increased expression of a significant number of IFN-stimulated genes (ISG). RT-PCR analysis of ISG transcripts in individual and pooled samples further corroborated these data, and indicated that levels decreased to near those of controls following successful therapy. Significantly enhanced FcγR-stimulated ROS production was subsequently achieved by priming control neutrophils with IFN-α/-β/-γ, but not LPS, and gene expression analysis indicated that exposure to the type I IFN (in particular IFN-α) better replicated the mRNA profile observed in vivo. Further studies demonstrated that plasma levels of IFN-α were significantly higher in samples from patients relative to unaffected controls. Following successful periodontitis treatment, plasma IFN-α levels, neutrophil ISG expression, and FcγR-stimulated neutrophil ROS output of patients, all decreased to levels comparable with those of controls. In conclusion, although chronic periodontitis is a complex disease, raised IFN-α may be one determinant of the distinct molecular phenotype and hyperresponsivity exhibited by patients’ peripheral blood neutrophils.

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Section: Discussionsupporting

confidence: 74%

Periodontitis Associates with a Type 1 IFN Signature in Peripheral Blood Neutrophils

Wright

Matthews

Chapple

et al. 2008

The Journal of Immunology

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“…Stimulation with Gram-negative bacteria including Salmonella typhimurium and Escherichia coli or LPS derived from these bacteria induces type I IFN production [102][103][104][105]. Other bacterial components that induce type I IFN include bacterial DNA and Gram-negative flagellin, indicating other bacterial infections may also activate type I IFN production [60,103].…”

Section: Type I Ifn Production In Response To Bacterial Infectionmentioning

confidence: 99%

The host type I interferon response to viral and bacterial infections

et al. 2005

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Type I interferons (IFN) are well studied cytokines with anti-viral and immune-modulating functions. Type I IFNs are produced following viral infections, but until recently, the mechanisms of viral recognition leading to IFN production were largely unknown. Toll like receptors (TLRs) have emerged as key transducers of type I IFN during viral infections by recognizing various viral components. Furthermore, much progress has been made in defining the signaling pathways downstream of TLRs for type I IFN production. TLR7 and TLR9 have become apparent as universally important in inducing type I IFN during infection with most viruses, particularly by plasmacytoid dendritic cells. New intracellular viral pattern recognition receptors leading to type I IFN production have been identified. Many bacteria can also induce the up-regulation of these cytokines. Interestingly, recent studies have found a detrimental effect on host cells if type I IFN is produced during infection with the intracellular gram-positive bacterial pathogen, Listeria monocytogenes. This review will discuss the recent advances made in defining the signaling pathways leading to type I IFN production.

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“…There are a few studies available that state that intracellular bacteria such as chlamydia, salmonella, mycobacteria, and listeria can induce type I IFN production (31)(32)(33)(34)(35)(36), while even fewer reports observe type I IFN secretion in response to extracellular bacteria including Staphylococcus aureus and Escherichia coli (37)(38)(39)(40). Although triggering innate immune cells other than pDC by primarily extracellularly located bacteria mainly occurs via cell wall-associated TLR2-active LP or endotoxin-mediated engagement of TLR4, there is little information on the molecular mechanisms involved in human pDC activation.…”

Section: P Lasmacytoid Dendritic Cells (Pdc)mentioning

confidence: 99%

Staphylococcus aureus-Induced Plasmacytoid Dendritic Cell Activation Is Based on an IgG-Mediated Memory Response

Parčina

Wendt

Goetz

et al. 2008

The Journal of Immunology

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Type I IFNs represent a major antimicrobial defense mechanism due to their property of enhancing immune responses by priming both innate and adaptive immune cells. Plasmacytoid dendritic cells (pDC) are the major source of type I IFN in the human body and represent innate immune cells involved in first-line defense against invading pathogens. Although pDC activation has been extensively studied upon stimulation with synthetic TLR ligands, viruses, and intracellular bacteria, there is only scarce information on extracellular bacteria. In this study we show that the triggering of human pDC-derived IFN-α secretion by Staphylococcus aureus is independent of TLR2 and specific for coagulase-positive staphylococci. Specificity of the pDC response to S. aureus is independent of the bacterial virulence factors protein A and α-toxin but is mediated by Ag-specific IgG and CD32. S. aureus-induced pDC activation can be blocked by inhibitory DNA oligonucleotides and chloroquine, suggesting that engagement of TLR7/9 by bacterial nucleic acids after CD32-mediated uptake of these compounds may play a central role in this process. Altogether, we propose that in marked contrast to nonselective TLR2-dependent activation of most innate immune cells, pDC activation by S. aureus represents an Ag-specific memory response since it requires the presence of class-switched immunoglobulins.

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Production of Interferon‐α/β by Murine Dendritic Cell Lines Stimulated by Virus and Bacteria

Cited by 40 publications

References 32 publications

Periodontitis Associates with a Type 1 IFN Signature in Peripheral Blood Neutrophils

Periodontitis Associates with a Type 1 IFN Signature in Peripheral Blood Neutrophils

The host type I interferon response to viral and bacterial infections

Staphylococcus aureus-Induced Plasmacytoid Dendritic Cell Activation Is Based on an IgG-Mediated Memory Response

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