Speculations on the activation of ROS generation in C. elegans innate immune signaling

Hoeven, Ransome van der; McCallum, Katie C.; Garsin, Danielle A.

doi:10.4161/worm.19767

Cited by 17 publications

(12 citation statements)

References 24 publications

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“…This connection between bacteria and the host has been studied extensively in the nematode worm Caenorhabditis elegans [76] , [77] , [78] , [79] , but as Elizabeth A. Veal and Antonio Miranda-Vizuete comment, C. elegans can serve as a general model for redox biology and has already provided significant new insight into the interplay between ROS, ROS signaling and aging. Notably, genetic studies have failed to show that the ROS-detoxifying activities of any of C. elegans ’ array of ROS-metabolizing enzymes protects against aging.…”

Section: Conceptual and Mechanistic Aspects Of Ros And Oxidative Strementioning

confidence: 99%

European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS)

et al. 2017

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The European Cooperation in Science and Technology (COST) provides an ideal framework to establish multi-disciplinary research networks. COST Action BM1203 (EU-ROS) represents a consortium of researchers from different disciplines who are dedicated to providing new insights and tools for better understanding redox biology and medicine and, in the long run, to finding new therapeutic strategies to target dysregulated redox processes in various diseases. This report highlights the major achievements of EU-ROS as well as research updates and new perspectives arising from its members. The EU-ROS consortium comprised more than 140 active members who worked together for four years on the topics briefly described below. The formation of reactive oxygen and nitrogen species (RONS) is an established hallmark of our aerobic environment and metabolism but RONS also act as messengers via redox regulation of essential cellular processes. The fact that many diseases have been found to be associated with oxidative stress established the theory of oxidative stress as a trigger of diseases that can be corrected by antioxidant therapy. However, while experimental studies support this thesis, clinical studies still generate controversial results, due to complex pathophysiology of oxidative stress in humans. For future improvement of antioxidant therapy and better understanding of redox-associated disease progression detailed knowledge on the sources and targets of RONS formation and discrimination of their detrimental or beneficial roles is required. In order to advance this important area of biology and medicine, highly synergistic approaches combining a variety of diverse and contrasting disciplines are needed.

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Section: Conceptual and Mechanistic Aspects Of Ros And Oxidative Strementioning

confidence: 99%

European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS)

et al. 2017

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“…Furthermore, C. elegans Gα q was recently shown to control both innate immunity and infection avoidance behavior against M. nematophilum (McMullan et al, 2012). In addition, DKF-2, which is paralogous to DKF-1, is controlled by PKCδ and is important in the intestine for p38 MAPK-mediated defense against Enterococcus faecalis and P. aeruginosa through dual oxidase (Duox) BLI-3 (Feng et al, 2007; van der Hoeven et al, 2011, 2012; Ren et al, 2009). Whether DKF-1 is also important for HLH-30 activation in animals infected with Enterococcus faecalis or P. aeruginosa , or whether this might be dependent on DKF-2 instead, remains to be determined.…”

Section: Discussionmentioning

confidence: 99%

An Evolutionarily Conserved PLC-PKD-TFEB Pathway for Host Defense

et al. 2016

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Summary The mechanisms that tightly control the transcription of host defense genes have not been fully elucidated. We previously identified TFEB as a transcription factor important for host defense, but the mechanisms that regulate TFEB during infection remained unknown. We used C. elegans to discover a pathway that activates TFEB during infection. Gene dkf-1, which encodes a homolog of protein kinase D (PKD), was required for TFEB activation in nematodes infected with Staphylococcus aureus. Conversely, pharmacological activation of PKD was sufficient to activate TFEB. Furthermore, phospholipase C (PLC) gene plc-1 was also required for TFEB activation, downstream of Gαq homolog egl-30 and upstream of dkf-1. Using reverse and chemical genetics, we discovered a similar PLC-PKD-TFEB axis in Salmonella-infected mouse macrophages. In addition, PKCα was required in macrophages but not nematodes. These observations reveal a previously unknown host defense signaling pathway, which has been conserved across one billion years of evolution.

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“…faecalis , it has been demonstrated that the NADPH oxidase domain of BLI-3 is critical for this protective function; the peroxidase domain does not appear to have a role [5,8]. While it is known that BLI-3 is not regulated at the mRNA or protein level, the infection-dependent signals and corresponding regulatory components that control the stimulation of BLI-3 during intestinal-specific infection remain unclear [8,15], though there is some evidence that bacterial-derived uracil modulates the process [16]. In the case of epidermal infection by D .…”

Section: Elegans Produces Ros Via Ce-duox1/bli-3 During the Immunementioning

confidence: 99%

The Role of Reactive Oxygen Species in Modulating the Caenorhabditis elegans Immune Response

McCallum

Garsin

2016

PLoS Pathog

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Speculations on the activation of ROS generation in C. elegans innate immune signaling

Cited by 17 publications

References 24 publications

European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS)

European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS)

An Evolutionarily Conserved PLC-PKD-TFEB Pathway for Host Defense

The Role of Reactive Oxygen Species in Modulating the Caenorhabditis elegans Immune Response

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