Neurogenic Inflammation

Inflammation caused by an injurious stimulus of peripheral neurons and resulting in release of neuropeptides which affect vascular permeability and help initiate proinflammatory and immune reactions at the site of injury.

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Networked: 986 relevant articles (20 outcomes, 102 trials/studies)

Relationship Network

Disease Context: Research Results

Related Diseases

1.	Pain (Aches)
2.	Inflammation
3.	Migraine Disorders (Migraine)
4.	Hyperalgesia
5.	Asthma (Bronchial Asthma)

Experts

1.	Geppetti, Pierangelo: 14 articles (07/2014 - 04/2004)
2.	Vink, Robert: 14 articles (01/2014 - 10/2004)
3.	Bunnett, Nigel W: 13 articles (11/2015 - 06/2004)
4.	Bhatia, Madhav: 10 articles (11/2011 - 05/2003)
5.	Nassini, Romina: 9 articles (07/2014 - 08/2007)
6.	Materazzi, Serena: 9 articles (07/2014 - 03/2006)
7.	Szolcsányi, János: 8 articles (05/2015 - 08/2002)
8.	Birklein, Frank: 8 articles (05/2014 - 07/2006)
9.	Lin, Qing: 8 articles (09/2010 - 02/2003)
10.	Szolcsányi, J: 8 articles (12/2008 - 12/2001)

Drugs and Biologics

Drugs and Important Biological Agents (IBA) related to Neurogenic Inflammation:

1.	Substance PIBA 06/14/2005 - "In this study, we performed a series of experiments to investigate whether substance P (SP) contributes to neurogenic inflammation in the skeletal muscle tissue. " 05/22/1992 - "Substance P-immunoreactive sensory axons in the rat respiratory tract: a quantitative study of their distribution and role in neurogenic inflammation." 09/01/2013 - "TRPA1 was expressed in vagal nerve afferents, and the TRPA1 antagonist significantly inhibited the expression of substance P, indicating the involvement of TRPA1 in neurogenic inflammation. " 03/01/2013 - "Substance P (SP), a mediator of neurogenic inflammation, is a key element of the striato-nigral circuitry, but alterations of SP in the SN have not been studied after acute striatal injury. " 01/01/2013 - "Accordingly, blocking substance P NK1 receptors may provide a novel alternative treatment to ameliorate the deleterious effects of neurogenic inflammation in the central nervous system. "
2.	Capsaicin (Zostrix)FDA Link 04/01/2006 - "In our previous study, deafferentation with pretreatment of the sciatic nerve with capsaicin, which reduces neurogenic inflammation and has a selective effect on nociceptive fibers, improved functional recovery of the muscle after I/R. " 06/01/2014 - "Capsaicin-induced neurogenic inflammation in pig skin: a behavioural study." 12/01/2006 - "The aim of this study was to evaluate the effects of topical capsaicin application on human lingual mucosa and to assess if neurogenic inflammation might have a role in the pathogenesis of lingual diseases. " 06/01/2006 - "Recent behavioral and electrophysiological studies have attributed an important role to dorsal root reflexes (DRRs) in the initiation and development of neurogenic inflammation produced by intradermal capsaicin (CAP). " 05/01/2006 - "In the present study, we examined the dynamic vasomotor balance of capsaicin-induced vasodilatation within the area of the induced neurogenic inflammation, with and without superimposed cooling. "
3.	NeuropeptidesIBA 01/01/2013 - "The objectives of this study were to establish SP metabolic stability in liver microsomes in three species (rat, mouse and human), and identify and characterize SP metabolites by LC-MS/MS. Endogenous peptide metabolism is not well documented and this is particularly true for neuropeptides participating in neurogenic inflammation. " 07/01/2009 - "This study investigated the underlying mechanisms of NPE, focusing on neuropeptides, which potently induce vasoconstriction, vasodilatation, and neurogenic inflammation. " 01/01/2003 - "However, few studies have examined the role of neuropeptide induced neurogenic inflammation following TBI. " 11/01/1997 - "Peripheral CGRP release as a marker for neurogenic inflammation: a model system for the study of neuropeptide secretion in rat paw skin." 06/01/1996 - "Extensive studies of neurogenic inflammation in rodents show that sensory neuropeptides can open gaps between the endothelial cells of postcapillary venules and the same change can be caused by a large number of inflammatory mediators. "
4.	Calcitonin Gene-Related PeptideIBA 11/01/2015 - "Peripheral release of calcitonin gene-related peptide (CGRP) contributes to the vasodilation of acute neurogenic inflammation. " 07/01/2015 - "Calcitonin gene-related peptide (CGRP) has been shown to induce motility disturbances and in addition may be a candidate mediator to elicit neurogenic inflammation. " 05/01/2014 - "We hypothesized that endodontic sealers can directly activate trigeminal nociceptors in a concentration-dependent manner, resulting in release of calcitonin gene-related peptide (CGRP), a potent modulator of neurogenic inflammation. " 07/01/2007 - "Calcitonin gene-related peptide (CGRP) mediates neurogenic inflammation and modulates intestinal motility. " 07/15/2003 - "Calcitonin gene-related peptide (CGRP) is synthesized in dorsal root ganglion (DRG) neurons and released from primary afferent neurons to mediate hemodynamic effects and neurogenic inflammation. "
5.	TachykininsIBA 08/01/1997 - "Others studies have also indicated that tachykinin NK1-receptors are involved in immediate or delayed neurogenic inflammation including microvascular leakage and the subsequent increase in plasma protein extravasation. " 12/01/1998 - "Airway neurogenic inflammation is caused by tachykinins released from peripheral nerve endings of sensory neurons within the airways, and is characterized by plasma protein extravasation, airway smooth muscle contraction and increased secretion of mucus. " 04/01/1997 - "Neurogenic inflammation is mediated by release of tachykinins from sensory nerves, which stimulate plasma extravasation from postcapillary venules. " 01/01/1995 - "In humans, tachykinins have been shown to increase plasma exudation in the nasal mucosa, but whether neurogenic inflammation also occurs in the lower airways still remains to be proven." 01/01/1995 - "In the peripheral nervous system, tachykinins released from peripheral endings of sensory nerves are responsible for the neurogenic inflammation phenomenon. "
6.	Serotonin (5 Hydroxytryptamine)IBA 06/01/1999 - "The efficacy of 5-hydroxytryptamine 1B/1D (5-HT 1B/1D) agonists is related to their inhibitory effects on neurogenic inflammation, mediated through serotoninergic control mechanisms. " 04/18/1997 - "Role of the 5-HT receptor in neurogenic inflammation in Fisher 344 rat airways." 08/01/2006 - "Their mechanisms of action include raising the threshold to migraine activation, enhancing antinociception, inhibiting cortical spreading depression, inhibiting peripheral and central sensitization, blocking neurogenic inflammation and modulating sympathetic, parasympathetic or 5-HT tone. " 03/01/1997 - "The novel antimigraine drug 311C90 (Zomig; zolmitriptan) has a high selectivity for serotonin (5HT)1 receptors, mainly 5HT1B and 5HT1D subtypes, and in preclinical studies it has been shown to act on four different sites within the trigemino-vascular system (blockade of neurogenic inflammation by inhibition of peptide release, vasoconstriction, inhibition of neuronal depolarization at peripheral sites, and effects at central sites). " 07/01/2000 - "The action of 5-hydroxytryptamine (5-HT1B/1D) agonists--so-called triptans--on receptors located in meningeal arteries (5-HT1B) and trigeminovascular fiber endings (5-HT1D) has an inhibitory effect on this neurogenic inflammation. "
7.	Histamine (Histamine Dihydrochloride)FDA Link 09/01/2013 - "The role of histamine in neurogenic inflammation." 10/01/2009 - "Findings from blood flow (F(1,26) = 177.3, P < 0.001) and temperature measurements (F(1,26) = 27.6, P < 0.001) clearly showed the suppressive effect of BoNT/A on vasomotor reactions, with the maximal effect on days 3 and 7. BoNT/A reduced the itch intensity, blood flow and neurogenic inflammation in response to the histamine prick test in human skin. " 01/01/2005 - "Via peripheral H3-receptors, histamine modulates neurogenic inflammation and via H4-receptors functions of immune cells. " 02/01/2004 - "These results indicate that exposure to VOC may enhance neurogenic inflammation with concomitant enhancement of histamine-induced responses." 05/01/1999 - "The time course of plasma extravasation and release of histamine and MCT from dermal mast cells in neurogenic inflammation was measured in vivo by intradermal microdialysis in humans. "
8.	Sumatriptan (Imigran)FDA LinkGeneric 11/01/2006 - "Sumatriptan, which is also effective in aborting CH attacks, is known to inhibit neurogenic inflammation of the dura mater. " 01/01/1997 - "These data suggest that sumatriptan inhibits neurogenic inflammation via 5-HT1D alpha receptors in guinea pigs and 5-HT1D beta (5-HT1B) receptors in rats. " 05/01/1996 - "Rat knee joint plasma extravasation was used to determine the effect of sumatriptan on peripheral neurogenic inflammation. " 11/01/1995 - "These data demonstrate that sumatriptan inhibits neurogenic inflammation in the rat (MED, 100 micrograms kg-1, i.v.), and produces vasoconstriction in the dog, over a similar dose-range. " 01/01/1994 - "Sumatriptan blocks neurogenic inflammation in the peripheral nerve trunk."
9.	SmokeIBA 03/01/2012 - "Recent studies have shown that neurogenic inflammation induced by cigarette smoke is inhibited by TRPA1 antagonist, but not by TRPV1 antagonist. " 12/01/1996 - "The results suggest that neurogenic inflammation and the subsequent generation of Tx in the airway are important in the development of the airway hyperresponsiveness induced by cigarette smoke." 12/01/1996 - "We investigated the role of neurogenic inflammation and the subsequent mechanisms in cigarette smoke-induced airway hyperresponsiveness in guinea pigs. " 12/01/1996 - "Thromboxane causes airway hyperresponsiveness after cigarette smoke-induced neurogenic inflammation." 07/01/2008 - "Cigarette smoke-induced neurogenic inflammation is mediated by alpha,beta-unsaturated aldehydes and the TRPA1 receptor in rodents."
10.	Complement System Proteins (Complement)IBA 01/01/2012 - "A new treatment for neurogenic inflammation caused by EV71 with CR2-targeted complement inhibitor." 01/01/1994 - "Peptidergic activation of mast cells may also be a pathophysiological process having an important role in neurogenic inflammation and in diseases involving extensive activation of the blood complement cascade." 11/01/1996 - "These studies complement prior experiments showing that valproic acid and allopregnanolone block neurogenic inflammation within the meninges via GABAA receptor-mediated mechanisms. " 03/01/2002 - "The authors review the available evidence linking these factors to the development of inflammatory lesions of the cerebral vasculature, emphasizing: 1) neurogenic inflammation due to massive release of sensory nerve neuropeptides; 2) hemoglobin from lysed erythrocytes, which creates functional lesions of endothelial and smooth muscle cells; 3) activity, expression and metabolites of lipoxygenases cyclooxygenases and nitric oxide synthases; 4) the possible role of endothelin-1 as a pro-inflammatory agent; 5) serotonin, histamine and bradykinin which are especially involved in blood-brain barrier disruption; 6) the prothrombotic and pro-inflammatory action of complement and thrombin towards endothelium; 7) the multiple actions of activated platelets, including platelet-derived growth factor production; 8) the presence of perivascular and intramural macrophages and granulocytes and their interaction with adhesion molecules; 9) the evolution, origins, and effects of pro-inflammatory cytokines, especially IL-1, TNF-alpha and IL-6. Human and animal studies on the use of anti-inflammatory agents in subarachnoid hemorrhage include superoxide and other radical scavengers, lipid peroxidation inhibitors, iron chelators, NSAIDs, glucocorticoids, and serine protease inhibitors. "

Therapies and Procedures

1.	Intradermal Injections 09/27/2010 - "Our previous studies suggest that neurogenic inflammation induced by intradermal injection of capsaicin results from the enhancement of dorsal root reflexes (DRRs), which involve antidromic activation of dorsal root ganglion (DRG) neurons. " 01/01/2004 - "In a recent study, we have demonstrated that the dorsal root reflex (DRR)-mediated acute cutaneous neurogenic inflammation following intradermal injection of capsaicin (CAP) is sympathetically dependent and subject to modulation by peripheral alpha(1)-adrenoceptors. " 01/01/2007 - "Here we used pharmacological manipulations to analyze the roles of TRPV1 and neuropeptidergic receptors in the DRR-mediated neurogenic inflammation induced by intradermal injection of capsaicin. " 01/01/2007 - "Acute cutaneous neurogenic inflammation initiated by activation of transient receptor potential vanilloid-1 (TRPV1) receptors following intradermal injection of capsaicin is mediated mainly by dorsal root reflexes (DRRs). " 01/01/2007 - "Roles of TRPV1 and neuropeptidergic receptors in dorsal root reflex-mediated neurogenic inflammation induced by intradermal injection of capsaicin."
2.	Intravenous Injections 06/24/2010 - "After SPA for 1 or 6 days, neurogenic inflammation was induced by intravenous injection of capsaicin (90microg/kg) or substance P (SP; 3microg/kg). " 03/01/1991 - "Neurogenic inflammation was evoked by an intravenous injection of capsaicin, and 5 min later the magnitude of the response was quantified by measuring the amount of extravasation of two tracers, Monastral blue pigment and Evans blue dye. " 06/01/1989 - "Neurogenic inflammation was produced by antidromic electrical stimulation of one vagus nerve (2.5 Hz, 1 ms, 5 V for 5 min) in the presence of atropine or by an intravenous injection of capsaicin (100 micrograms/kg). " 12/10/2001 - "One week later in our procedure, we investigated if neurogenic inflammation induced by an intravenous injection of capsaicin (300 nmol/ml/kg) and innervation density of substance P-immunoreactive sensory axons could be decreased after chronic denervation in the rat lower airways. " 02/01/1996 - "Bosentan was effective for preventing neurogenic inflammation in the dura mater induced by unilateral electrical stimulation of the trigeminal ganglion or intravenous injection of capsaicin, whereas it was ineffective in extracranial tissues or after injection of substance P (non-neurogenic inflammation). "
3.	Nerve Block (Nerve Blocks) 05/01/2010 - "This may partly explain the efficacy of nerve blocks with bupivacaine to decrease the neurogenic inflammation and in a lower extent the long-term inhibition of hyperalgesic phenomenon observed in animals and in humans."
4.	Subcutaneous Injections 01/01/1990 - "Subcutaneous injection of 50 mg/kg capsaicin to newborn rats resulted in a marked decrease of heat pain sensitivity and neurogenic inflammation. "
5.	Lasers (Laser) 10/01/2009 - "The itch intensity (as rated on a 0-10 visual analogue scale), itch area, neurogenic inflammation (visible flare area), blood flow (laser Doppler) and cutaneous temperature (thermographic images) were measured over the course of the trials. " 07/01/2006 - "Vasodilator axon reflexes ("neurogenic" inflammation) were quantified by laser-Doppler-imaging and served as surrogates for primary afferent activation. " 09/01/2003 - "However, recent developments of thermography and laser-Doppler flowmetry have facilitated quantitative measurement of the neurogenic inflammation. " 01/01/1993 - "Neurogenic inflammation was assessed by laser Doppler flowmetry and by planimetry of flare sizes. " 01/01/1992 - "Using the micropuncture technique and laser Doppler flowmetry we have performed simultaneous measurements of tissue pressure and blood flow in the cat dental pulp during neurogenic inflammation. "