Immune Activation of Type I IFNs by <i>Listeria monocytogenes</i> Occurs Independently of TLR4, TLR2, and Receptor Interacting Protein 2 but Involves TANK-Binding Kinase 1

O’Connell, Ryan M.; Vaidya, Sagar A.; Perry, Andrea K.; Saha, Supriya K.; Dempsey, Paul W.; Cheng, Genhong

doi:10.4049/jimmunol.174.3.1602

Cited by 82 publications

(89 citation statements)

References 35 publications

(48 reference statements)

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“…The results presented here argue that Nod proteins do not significantly influence the activation of the type I IFN pathway mediated by this unidentified bacterial DNA sensor. This is in agreement with a previous study which demonstrated that intracellular detection of invasive bacteria results in the activation of the type I IFN responses, independently of receptor-interacting protein 2, a critical adaptor protein acting downstream of Nod1 and Nod2 [27].…”

Section: Discussionsupporting

confidence: 94%

Nod1 and Nod2 induce CCL5/RANTES through the NF‐κB pathway

et al. 2007

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The Nod-like receptor proteins Nod1 and Nod2 participate in innate immune responses against bacteria through intracellular detection of peptidoglycan, a component of bacterial cell wall. Recent evidence has demonstrated that Nod1 stimulates the release of chemokines that attract neutrophils at the site of infection, such as CXCL8/IL-8 in humans, and CXCL1/keratinocyte-derived chemokine and CXCL2/MIP-2 in mice. We aimed to determine whether Nod proteins could trigger the release of CCL5/RANTES, a chemokine known to attract a number of immune cells, but not neutrophils. Our results demonstrate that activation of both Nod1 and Nod2 results in substantial secretion of CCL5 by murine macrophages. Moreover, in vivo, the intraperitoneal injection of murine Nod1 or Nod2 agonists resulted in a rapid secretion of CCL5 into the bloodstream. We also observed that Nod-dependent secretion of CCL5 did not correlate with the induction of the interferon-b pathway, a major signaling cascade for the activation of CCL5 by viruses. In contrast, we identified a key role of the NF-jB pathway in Noddependent stimulation of the CCL5 promoter. Together, these results identify a novel target downstream of Nod1 and Nod2, which is likely to play a key role in orchestrating the global Nod-dependent immune defense during bacterial infections.

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Section: Discussionsupporting

confidence: 94%

Nod1 and Nod2 induce CCL5/RANTES through the NF‐κB pathway

et al. 2007

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“…As shown in Fig. 6A, LM infection resulted in increased serum levels of IFN-␤ that peaked at 48 h after infection and were similar in WT and MyD88 Ϫ/Ϫ mice, confirming previous reports that IFN-␤ production by LM is MyD88 independent (25). IFN-␤ serum levels were not increased in LM-infected IFN␣R1 Ϫ/Ϫ mice (Fig.…”

Section: Prevention Of Tolerance By Lm Infection Is Mediated By Type supporting

confidence: 76%

“…The invasion of the cytosol triggers early inflammatory responses and, ultimately, protective immunity that depends both on innate and adaptive immune responses. Innate immune events include the production of MCP-1 (CCL2) and type I IFNs in a MyD88-independent but NF-B-dependent, manner (25). The secretion of MCP-1 by LM-infected cells results in the emigration of neutrophils and blood CD11b ϩ monocytes out of the bone marrow (26).…”

Section: Linical Data Support a Correlation Between Viral Infectionsmentioning

confidence: 99%

Prevention of Allograft Tolerance by Bacterial Infection with Listeria monocytogenes

Wang¹,

Chen

Ahmed³

et al. 2008

The Journal of Immunology

101

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Exposure to certain viruses and parasites has been shown to prevent the induction of transplantation tolerance in mice via the generation of cross-reactive memory T cell responses or the induction of bystander activation. Bacterial infections are common in the perioperative period of solid organ allograft recipients in the clinic, and correlations between bacterial infections and acute allograft rejection have been reported. However, whether bacterial infections at the time of transplantation have any effect on the generation of transplantation tolerance remains to be established. We used the Gram-positive intracellular bacterium Listeria monocytogenes (LM) as a model pathogen because its effects on immune responses are well described. Perioperative LM infection prevented cardiac and skin allograft acceptance induced by anti-CD154 and donor-specific transfusion in mice. LM-mediated rejection was not due to the generation of cross-reactive T cells and was largely independent of signaling via MyD88, an adaptor for most TLRs, IL-1, and IL-18. Instead, transplant rejection following LM infection was dependent on the expression of the phagosome-lysing pore former listeriolysin O and on type I IFN receptor signaling. Our results indicate that bacterial exposure at the time of transplantation can antagonize tolerogenic regimens by enhancing alloantigen-specific immune responses independently of the generation of cross-reactive memory T cells.

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“…This unique property of LLO may be essential for the intracellular parasitism of L. monocytogenes. Activation of LLO by acidification of phagosomes containing L. monocytogenes is an important step in bacterial escape because the inhibition of phagosomal acidification by H + -ATPase inhibitors, bafilomycin A 1 or concanamycin A, results in the prevention of bacterial escape into the cytoplasm (Beauregard et al, 1997;O'Connell et al, 2005). Also, functional inactivation at a neutral pH is likely essential for intracellular parasitism of this bacterium.…”

Section: Introductionmentioning

confidence: 99%

Irreversible loss of membrane-binding activity of Listeria-derived cytolysins in non-acidic conditions: a distinct difference from allied cytolysins produced by other Gram-positive bacteria

et al. 2007

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Listeriolysin O (LLO), a member of the cholesterol-dependent cytolysin (CDC) family, is a major virulence factor of Listeria monocytogenes and contributes to bacterial escape from intracellular killing of macrophages. LLO is activated under weakly acidic conditions; however, the molecular mechanism of this pH-dependent expression of cytolytic activity of LLO is poorly understood. In this study, CDCs including LLO, ivanolysin O (ILO), seeligeriolysin O (LSO), pneumolysin (PLY), streptolysin O (SLO) and perfringolysin O (PFO) were prepared as recombinant proteins and examined for their functional changes after treatment under various pH conditions. Haemolytic and membrane cholesterol-binding activities were not affected in PLY, SLO and PFO at any pH examined. By contrast, all the Listeria-derived cytolysins, LLO, ILO and LSO, were active only at an acidic pH and rapidly inactivated under neutral or alkaline conditions. Once inactivated, LLO could not be reactivated even by a downward pH shift. The hydrophobicity of LLO treated at neutral or alkaline pH was increased. These data suggested that the pHdependent loss of cytolytic activity appeared to be due to irreversible structural changes of domain 4 that resulted in the loss of target membrane cholesterol binding.

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Immune Activation of Type I IFNs by Listeria monocytogenes Occurs Independently of TLR4, TLR2, and Receptor Interacting Protein 2 but Involves TANK-Binding Kinase 1

Cited by 82 publications

References 35 publications

Nod1 and Nod2 induce CCL5/RANTES through the NF‐κB pathway

Nod1 and Nod2 induce CCL5/RANTES through the NF‐κB pathway

Prevention of Allograft Tolerance by Bacterial Infection with Listeria monocytogenes

Irreversible loss of membrane-binding activity of Listeria-derived cytolysins in non-acidic conditions: a distinct difference from allied cytolysins produced by other Gram-positive bacteria

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