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Article ; Online: Reply to: Neuroimmune interactions and COVID-19 in lung transplant recipients.

De Virgiliis, Francesco / Di Giovanni, Simone

2021 Volume 17, Issue 5, Page(s) 325–326

MeSH term(s)	COVID-19 ; Cytokine Release Syndrome ; Humans ; Lung ; Neuroimmunomodulation ; SARS-CoV-2 ; Transplant Recipients
Language	English
Publishing date	2021-03-24
Publishing country	England
Document type	Letter ; Comment
ZDB-ID	2491514-2
ISSN	1759-4766 ; 1759-4758
ISSN (online)	1759-4766
ISSN	1759-4758
DOI	10.1038/s41582-021-00485-w
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Article ; Online: Control of lymph node activity by direct local innervation.

De Virgiliis, Francesco / Oliva, Valeria Maria / Kizil, Burak / Scheiermann, Christoph

Trends in neurosciences

2022 Volume 45, Issue 9, Page(s) 704–712

Abstract: The nervous system detects environmental and internal stimuli and relays this information to immune cells via neurotransmitters and neuropeptides. This is essential to respond appropriately to immunogenic threats and to support system homeostasis. Lymph ... ...

Abstract	The nervous system detects environmental and internal stimuli and relays this information to immune cells via neurotransmitters and neuropeptides. This is essential to respond appropriately to immunogenic threats and to support system homeostasis. Lymph nodes (LNs) act as sentinels where adaptive immune responses are generated. They are richly innervated by peripheral sympathetic and sensory nerves, which are responsible for the local secretion of neurotransmitters by sympathetic fibers, such as norepinephrine, and neuropeptides by sensory fibers, including calcitonin gene-related peptide (CGRP) and substance P. Additionally, time-of-day-dependent oscillations in nerve activity are associated with differential immune responses, suggesting a potential role for neuroimmune interactions in coordinating immunity in a circadian fashion. Here, we discuss how LN activity is controlled by local innervation.
MeSH term(s)	Calcitonin Gene-Related Peptide ; Humans ; Lymph Nodes/innervation ; Neuropeptides ; Neurotransmitter Agents ; Substance P
Chemical Substances	Neuropeptides ; Neurotransmitter Agents ; Substance P (33507-63-0) ; Calcitonin Gene-Related Peptide (JHB2QIZ69Z)
Language	English
Publishing date	2022-07-09
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	282488-7
ISSN	1878-108X ; 0378-5912 ; 0166-2236
ISSN (online)	1878-108X
ISSN	0378-5912 ; 0166-2236
DOI	10.1016/j.tins.2022.06.006
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Article ; Online: Lung innervation in the eye of a cytokine storm: neuroimmune interactions and COVID-19.

De Virgiliis, Francesco / Di Giovanni, Simone

Nature reviews. Neurology

2020 Volume 16, Issue 11, Page(s) 645–652

Abstract: COVID-19 is an infectious disease caused by the coronavirus SARS-CoV-2, which was first reported in Wuhan, China, in December 2019 and has caused a global pandemic. Acute respiratory distress syndrome (ARDS) is a common feature of severe forms of COVID- ... ...

Abstract	COVID-19 is an infectious disease caused by the coronavirus SARS-CoV-2, which was first reported in Wuhan, China, in December 2019 and has caused a global pandemic. Acute respiratory distress syndrome (ARDS) is a common feature of severe forms of COVID-19 and can lead to respiratory failure, especially in older individuals. The increasing recognition of the neurotropic potential of SARS-CoV-2 has sparked interest in the role of the nervous system in respiratory failure in people with COVID-19. However, the neuroimmune interactions in the lung in the context of ARDS are poorly understood. In this Perspectives article, we propose the concept of the neuroimmune unit as a critical determinant of lung function in the context of COVID-19, inflammatory conditions and ageing, focusing particularly on the involvement of the vagus nerve. We discuss approaches such as neurostimulation and pharmacological neuromodulation to reduce tissue inflammation with the aim of preventing respiratory failure.
MeSH term(s)	Betacoronavirus ; COVID-19 ; Coronavirus Infections/complications ; Cytokine Release Syndrome/etiology ; Humans ; Lung/immunology ; Lung/innervation ; Neuroimmunomodulation/physiology ; Pandemics ; Pneumonia, Viral/complications ; Respiratory Insufficiency/etiology ; SARS-CoV-2
Keywords	covid19
Language	English
Publishing date	2020-08-25
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2491514-2
ISSN	1759-4766 ; 1759-4758
ISSN (online)	1759-4766
ISSN	1759-4758
DOI	10.1038/s41582-020-0402-y
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Article ; Online: Lung innervation in the eye of a cytokine storm

De Virgiliis, Francesco / Di Giovanni, Simone

Nature Reviews Neurology ; ISSN 1759-4758 1759-4766

neuroimmune interactions and COVID-19

2020

Keywords	Cellular and Molecular Neuroscience ; Clinical Neurology ; covid19
Language	English
Publisher	Springer Science and Business Media LLC
Publishing country	us
Document type	Article ; Online
DOI	10.1038/s41582-020-0402-y
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Lung innervation in the eye of a cytokine storm: neuroimmune interactions and COVID-19

De Virgiliis, Francesco / Di Giovanni, Simone

Nat Rev Neurol

Abstract	COVID-19 is an infectious disease caused by the coronavirus SARS-CoV-2, which was first reported in Wuhan, China, in December 2019 and has caused a global pandemic. Acute respiratory distress syndrome (ARDS) is a common feature of severe forms of COVID-19 and can lead to respiratory failure, especially in older individuals. The increasing recognition of the neurotropic potential of SARS-CoV-2 has sparked interest in the role of the nervous system in respiratory failure in people with COVID-19. However, the neuroimmune interactions in the lung in the context of ARDS are poorly understood. In this Perspectives article, we propose the concept of the neuroimmune unit as a critical determinant of lung function in the context of COVID-19, inflammatory conditions and ageing, focusing particularly on the involvement of the vagus nerve. We discuss approaches such as neurostimulation and pharmacological neuromodulation to reduce tissue inflammation with the aim of preventing respiratory failure.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #735551
Database	COVID19

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Article ; Online: Paracrine Mechanisms of Redox Signalling for Postmitotic Cell and Tissue Regeneration.

Hervera, Arnau / Santos, Celio X / De Virgiliis, Francesco / Shah, Ajay M / Di Giovanni, Simone

Trends in cell biology

2019 Volume 29, Issue 6, Page(s) 514–530

Abstract: Adult postmitotic mammalian cells, including neurons and cardiomyocytes, have a limited capacity to regenerate after injury. Therefore, an understanding of the molecular mechanisms underlying their regenerative ability is critical to advance tissue ... ...

Abstract	Adult postmitotic mammalian cells, including neurons and cardiomyocytes, have a limited capacity to regenerate after injury. Therefore, an understanding of the molecular mechanisms underlying their regenerative ability is critical to advance tissue repair therapies. Recent studies highlight how redox signalling via paracrine cell-to-cell communication may act as a central mechanism coupling tissue injury with regeneration. Post-injury redox paracrine signalling can act by diffusion to nearby cells, through mitochondria or within extracellular vesicles, affecting specific intracellular targets such as kinases, phosphatases, and transcription factors, which in turn trigger a regenerative response. Here, we review redox paracrine signalling mechanisms in postmitotic tissue regeneration and discuss current challenges and future directions.
MeSH term(s)	Animals ; Extracellular Vesicles/metabolism ; Humans ; Mitosis ; Myocytes, Cardiac/cytology ; Myocytes, Cardiac/metabolism ; Neurons/cytology ; Neurons/metabolism ; Oxidation-Reduction ; Paracrine Communication ; Signal Transduction
Language	English
Publishing date	2019-02-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	30122-x
ISSN	1879-3088 ; 0962-8924
ISSN (online)	1879-3088
ISSN	0962-8924
DOI	10.1016/j.tcb.2019.01.006
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Article ; Online: CBP/p300 activation promotes axon growth, sprouting, and synaptic plasticity in chronic experimental spinal cord injury with severe disability.

Müller, Franziska / De Virgiliis, Francesco / Kong, Guiping / Zhou, Luming / Serger, Elisabeth / Chadwick, Jessica / Sanchez-Vassopoulos, Alexandros / Singh, Akash Kumar / Eswaramoorthy, Muthusamy / Kundu, Tapas K / Di Giovanni, Simone

PLoS biology

2022 Volume 20, Issue 9, Page(s) e3001310

Abstract: The interruption of spinal circuitry following spinal cord injury (SCI) disrupts neural activity and is followed by a failure to mount an effective regenerative response resulting in permanent neurological disability. Functional recovery requires the ... ...

Abstract	The interruption of spinal circuitry following spinal cord injury (SCI) disrupts neural activity and is followed by a failure to mount an effective regenerative response resulting in permanent neurological disability. Functional recovery requires the enhancement of axonal and synaptic plasticity of spared as well as injured fibres, which need to sprout and/or regenerate to form new connections. Here, we have investigated whether the epigenetic stimulation of the regenerative gene expression program can overcome the current inability to promote neurological recovery in chronic SCI with severe disability. We delivered the CBP/p300 activator CSP-TTK21 or vehicle CSP weekly between week 12 and 22 following a transection model of SCI in mice housed in an enriched environment. Data analysis showed that CSP-TTK21 enhanced classical regenerative signalling in dorsal root ganglia sensory but not cortical motor neurons, stimulated motor and sensory axon growth, sprouting, and synaptic plasticity, but failed to promote neurological sensorimotor recovery. This work provides direct evidence that clinically suitable pharmacological CBP/p300 activation can promote the expression of regeneration-associated genes and axonal growth in a chronic SCI with severe neurological disability.
MeSH term(s)	Animals ; Axons/metabolism ; Mice ; Nerve Regeneration/physiology ; Neuronal Plasticity/physiology ; Recovery of Function/physiology ; Spinal Cord Injuries/metabolism
Language	English
Publishing date	2022-09-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2126776-5
ISSN	1545-7885 ; 1544-9173
ISSN (online)	1545-7885
ISSN	1544-9173
DOI	10.1371/journal.pbio.3001310
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Article ; Online: The circadian clock time tunes axonal regeneration.

De Virgiliis, Francesco / Mueller, Franziska / Palmisano, Ilaria / Chadwick, Jessica Sarah / Luengo-Gutierrez, Lucia / Giarrizzo, Angela / Yan, Yuyang / Danzi, Matt Christopher / Picon-Muñoz, Carmen / Zhou, Luming / Kong, Guiping / Serger, Elisabeth / Hutson, Thomas Haynes / Maldonado-Lasuncion, Ines / Song, Yayue / Scheiermann, Christoph / Brancaccio, Marco / Di Giovanni, Simone

Cell metabolism

2023 Volume 35, Issue 12, Page(s) 2153–2164.e4

Abstract: Nerve injuries cause permanent neurological disability due to limited axonal regeneration. Injury-dependent and -independent mechanisms have provided important insight into neuronal regeneration, however, common denominators underpinning regeneration ... ...

Abstract	Nerve injuries cause permanent neurological disability due to limited axonal regeneration. Injury-dependent and -independent mechanisms have provided important insight into neuronal regeneration, however, common denominators underpinning regeneration remain elusive. A comparative analysis of transcriptomic datasets associated with neuronal regenerative ability revealed circadian rhythms as the most significantly enriched pathway. Subsequently, we demonstrated that sensory neurons possess an endogenous clock and that their regenerative ability displays diurnal oscillations in a murine model of sciatic nerve injury. Consistently, transcriptomic analysis showed a time-of-day-dependent enrichment for processes associated with axonal regeneration and the circadian clock. Conditional deletion experiments demonstrated that Bmal1 is required for neuronal intrinsic circadian regeneration and target re-innervation. Lastly, lithium enhanced nerve regeneration in wild-type but not in clock-deficient mice. Together, these findings demonstrate that the molecular clock fine-tunes the regenerative ability of sensory neurons and propose compounds affecting clock pathways as a novel approach to nerve repair.
MeSH term(s)	Mice ; Animals ; Circadian Clocks/genetics ; Circadian Rhythm ; Nerve Regeneration/physiology ; Sensory Receptor Cells ; ARNTL Transcription Factors/genetics
Chemical Substances	ARNTL Transcription Factors
Language	English
Publishing date	2023-11-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2023.10.012
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Article ; Online: Reversible CD8 T cell-neuron cross-talk causes aging-dependent neuronal regenerative decline.

Zhou, Luming / Kong, Guiping / Palmisano, Ilaria / Cencioni, Maria Teresa / Danzi, Matt / De Virgiliis, Francesco / Chadwick, Jessica S / Crawford, Greg / Yu, Zicheng / De Winter, Fred / Lemmon, Vance / Bixby, John / Puttagunta, Radhika / Verhaagen, Joost / Pospori, Constandina / Lo Celso, Cristina / Strid, Jessica / Botto, Marina / Di Giovanni, Simone

Science (New York, N.Y.)

2022 Volume 376, Issue 6594, Page(s) eabd5926

Abstract: Aging is associated with increased prevalence of axonal injuries characterized by poor regeneration and disability. However, the underlying mechanisms remain unclear. In our experiments, RNA sequencing of sciatic dorsal root ganglia (DRG) revealed ... ...

Abstract	Aging is associated with increased prevalence of axonal injuries characterized by poor regeneration and disability. However, the underlying mechanisms remain unclear. In our experiments, RNA sequencing of sciatic dorsal root ganglia (DRG) revealed significant aging-dependent enrichment in T cell signaling both before and after sciatic nerve injury (SNI) in mice. Lymphotoxin activated the transcription factor NF-κB, which induced expression of the chemokine CXCL13 by neurons. This in turn recruited CXCR5
MeSH term(s)	Aging/metabolism ; Animals ; Axons/physiology ; CD8-Positive T-Lymphocytes/metabolism ; Ganglia, Spinal/metabolism ; Mice ; Nerve Regeneration ; Neurons/metabolism ; Sciatic Nerve/injuries ; Sciatic Nerve/physiology
Language	English
Publishing date	2022-05-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	128410-1
ISSN	1095-9203 ; 0036-8075
ISSN (online)	1095-9203
ISSN	0036-8075
DOI	10.1126/science.abd5926
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Article ; Online: The gut metabolite indole-3 propionate promotes nerve regeneration and repair.

Serger, Elisabeth / Luengo-Gutierrez, Lucia / Chadwick, Jessica S / Kong, Guiping / Zhou, Luming / Crawford, Greg / Danzi, Matt C / Myridakis, Antonis / Brandis, Alexander / Bello, Adesola Temitope / Müller, Franziska / Sanchez-Vassopoulos, Alexandros / De Virgiliis, Francesco / Liddell, Phoebe / Dumas, Marc Emmanuel / Strid, Jessica / Mani, Sridhar / Dodd, Dylan / Di Giovanni, Simone

Nature

2022 Volume 607, Issue 7919, Page(s) 585–592

Abstract: The regenerative potential of mammalian peripheral nervous system neurons after injury is critically limited by their slow axonal regenerative ... ...

Abstract	The regenerative potential of mammalian peripheral nervous system neurons after injury is critically limited by their slow axonal regenerative rate
MeSH term(s)	Animals ; Mice ; Axons/drug effects ; Axons/physiology ; Chemotaxis, Leukocyte ; Clostridium/metabolism ; Fasting ; Ganglia, Spinal/metabolism ; Gastrointestinal Microbiome ; Indoles/blood ; Indoles/metabolism ; Indoles/pharmacology ; Nerve Crush ; Nerve Growth Factors/metabolism ; Nerve Regeneration/drug effects ; Neutrophils/cytology ; Neutrophils/immunology ; Propionates/blood ; Propionates/metabolism ; Propionates/pharmacology ; Recovery of Function ; Sciatic Nerve/injuries ; Sequence Analysis, RNA ; Wound Healing/drug effects
Chemical Substances	Indoles ; Nerve Growth Factors ; Propionates ; indole-3 propionate
Language	English
Publishing date	2022-06-22
Publishing country	England
Document type	Journal Article
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-022-04884-x
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