Vagus nerve controls resolution and pro-resolving mediators of inflammation

Mirakaj, Valbona; Dalli, Jesmond; Granja, Tiago; Rosenberger, Peter; Serhan, Charles N.

doi:10.1084/jem.20132103

Cited by 148 publications

(157 citation statements)

References 32 publications

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“…Previous work also suggested that the administration of netrin 1 inhibits inflammation in several models of animal disease (36,37), but in our CIA mice, an anti-inflammatory effect of netrin 1 was not detected. Indeed, netrin 1 may not always exhibit anti-inflammatory activity, and contradictory results have been reported.…”

Section: Role Of Netrin 1 In Bone Homeostasiscontrasting

confidence: 83%

Bone-protective Functions of Netrin 1 Protein

Maruyama

Kawasaki

Hamaguchi³

et al. 2016

Journal of Biological Chemistry

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Edited by Amanda FosangNetrin 1 was initially identified as an axon guidance factor, and recent studies indicate that it inhibits chemokine-directed monocyte migration. Despite its importance as a neuroimmune guidance cue, the role of netrin 1 in osteoclasts is largely unknown. Here we detected high netrin 1 levels in the synovial fluid of rheumatoid arthritis patients. Netrin 1 is potently expressed in osteoblasts and synovial fibroblasts, and IL-17 robustly enhances netrin 1 expression in these cells. The binding of netrin 1 to its receptor UNC5b on osteoclasts resulted in activation of SHP1, which inhibited VAV3 phosphorylation and RAC1 activation. This significantly impaired the actin polymerization and fusion, but not the differentiation of osteoclast. Strikingly, netrin 1 treatment prevented bone erosion in an autoimmune arthritis model and age-related bone destruction. Therefore, the netrin 1-UNC5b axis is a novel therapeutic target for bone-destructive diseases.

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Section: Role Of Netrin 1 In Bone Homeostasiscontrasting

confidence: 83%

Bone-protective Functions of Netrin 1 Protein

Maruyama

Kawasaki

Hamaguchi³

et al. 2016

Journal of Biological Chemistry

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“…36 Furthermore, vagal denervation promotes persistent inflammation through failure to regulate resolution of inflammation. 37 The triad of inflammation, oxidative stress, and impaired baroreflex sensitivity is well recognized in the chronic development of cardiometabolic disease. 38 In conscious rats, loss of baroreflex function impedes attenuation of peripheral ( joint) inflammation, mediated by sympathetic neural drive.…”

Section: Discussionmentioning

confidence: 99%

Baroreflex impairment and morbidity after major surgery

Toner

Jenkins

Ackland

2016

British Journal of Anaesthesia

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Background: Baroreflex dysfunction is a common feature of established cardiometabolic diseases that are most frequently associated with the development of critical illness. Laboratory models show that baroreflex dysfunction impairs cardiac contractility and cardiovascular performance, thereby increasing the risk of morbidity after trauma and sepsis. We hypothesized that baroreflex dysfunction contributes to excess postoperative morbidity after major surgery as a consequence of the inability to achieve adequate perioperative tissue oxygen delivery. Methods: In a randomized controlled trial of goal-directed haemodynamic therapy (GDT) in higher-risk surgical patients, baroreflex function was assessed using the spontaneous baroreflex sensitivity (BRS) method via an arterial line placed before surgery, using a validated sequence method technique (one beat lag). The BRS was calculated during the 6 h postoperative GDT intervention. Analyses of BRS were done by investigators blinded to clinical outcomes. The primary outcome was the association between postoperative baroreflex dysfunction (BRS <6 mm Hg s −1 , a negative prognostic threshold in cardiovascular

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“…71 Importantly, the regulation of pro-resolving mediators appear to be influenced by neuronal functioning and may be reduced after neuronal injury and dysfunction associated with a reduction in Netrin-1 affecting resolvin D1 production. 72 Figure 3 (a) Normal nociceptor response to a noxious stimulus is shown. (b) Neuroplasticity in the first-order neuron (peripheral sensitization).…”

Section: Peripheral Sensitizationmentioning

confidence: 99%

Neuropathic ocular pain: an important yet underevaluated feature of dry eye

Galor

Levitt

Felix

et al. 2014

Eye

185

187

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Dry eye has gained recognition as a public health problem given its prevalence, morbidity, and cost implications. Dry eye can have a variety of symptoms including blurred vision, irritation, and ocular pain. Within dry eyeassociated ocular pain, some patients report transient pain whereas others complain of chronic pain. In this review, we will summarize the evidence that chronicity is more likely to occur in patients with dysfunction in their ocular sensory apparatus (ie, neuropathic ocular pain). Clinical evidence of dysfunction includes the presence of spontaneous dysesthesias, allodynia, hyperalgesia, and corneal nerve morphologic and functional abnormalities. Both peripheral and central sensitizations likely play a role in generating the noted clinical characteristics. We will further discuss how evaluating for neuropathic ocular pain may affect the treatment of dry eye-associated chronic pain.

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Vagus nerve controls resolution and pro-resolving mediators of inflammation

Abstract: Axonal guidance molecule netrin-1 promotes resolution of inflammation, with netrin-1 and resolvin D1 mutually inducing each other’s expression.

Cited by 148 publications

References 32 publications

Bone-protective Functions of Netrin 1 Protein

Bone-protective Functions of Netrin 1 Protein

Baroreflex impairment and morbidity after major surgery

Neuropathic ocular pain: an important yet underevaluated feature of dry eye

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