Neurogenic inflammation

Source: Wikipedia, the free encyclopedia.

Neurogenic inflammation is

endothelin-3 (ET-3).[1][2][3] In such neurons, release of these pro-inflammatory mediators is thought to be triggered by the activation of ion channels that are the principal detectors of noxious environmental stimuli. In particular, the heat/capsaicin receptor TRPV1[4] and the irritant/wasabi receptor TRPA1.[5][6][7] TRPA1 channels stimulated by lipopolysaccharide (LPS) may also cause acute neurogenic inflammation.[8]
Once released, these neuropeptides induce the release of histamine from adjacent mast cells. In turn, histamine evokes the release of substance P and calcitonin gene-related peptide; thus, a bidirectional link between histamine and neuropeptides in neurogenic inflammation is established.[9]

Neurogenic inflammation appears to play an important role in the

eczema, rosacea, dystonia, and multiple chemical sensitivity
. [17][18][19]

In

CGRP.[20][21] leading to a "sterile neurogenic inflammation."[22]

Prevention

Interleukin-1 beta (IL-1β), followed by exacerbated bone loss. These and other data suggest that deficient dietary magnesium intake, even at levels not uncommon in humans, may trigger neurogenic inflammation and lead to an increased risk of osteoporosis.[24]

Treatment

In 2018, three CGRP blockers were approved by the

FDA
for the prevention of migraine: erenumab; fremanezumab; and galcanezumab.

The calcitonin gene-related peptide (CGRP) is a therapeutic target in migraine because of its hypothesized role in mediating trigeminovascular pain transmission and the vasodilatory component of neurogenic inflammation (see "Pathophysiology, clinical manifestations, and diagnosis of migraine in adults", section on 'Role of calcitonin gene-related peptide'). In 2018, the US Food and Drug Administration (FDA) approved the CGRP antagonists erenumab [36], fremanezumab [37], and galcanezumab [38] for migraine prevention.
Smith, "Preventive treatment of migraine in adults" UpToDate 2019[25]

Additional CGRP blockers are progressing through clinical trials.[26]

Anticipating later

botox therapy for migraine, early work by Jancsó et al. found some success in treatment using denervation or pretreatment with capsaicin to prevent uncomfortable symptoms of neurogenic inflammation.[27]

A 2010 study of the treatment of migraine with CGRP blockers had shown promise for CGRP blockers.[28] In early trials, the first oral nonpeptide CGRP antagonist, MK-0974 (Telcagepant), was shown effective in the treatment of migraine attacks,[29] but elevated liver enzymes in two participants were found. Other therapies and other links in the neurogenic inflammatory pathway for interruption of disease are under study, including migraine therapies.[30]

Noting that botulinum toxin has been shown to have an effect on inhibiting neurogenic inflammation, and evidence suggesting the role of neurogenic inflammation in the pathogenesis of psoriasis,[14] the University of Minnesota has a pilot clinical trial underway to follow up on the observation that patients treated with botulinum toxin for dystonia had dramatic improvement in psoriasis.[31]

Astelin (

vasomotor rhinitis including rhinorrhea, nasal congestion, and post nasal drip in adults and children 12 years of age and older."[32][33]

Statins appear to "decrease expression of the proinflammatory neuropeptides calcitonin gene-related peptide and substance P in sensory neurons,"[34]
and so might be of use in treating diseases presenting with predominant neurogenic inflammation.

Research

In a 2012 article[35] in Nature Neuroscience Chiu et al. discuss the development of science related to neurogenic inflammation and provide a graphic[36] illustrating key discoveries leading toward the current understanding of neurogenic inflammation, its mechanisms, and the conditions caused by its disorder.

References

  1. ^
    PMID 16249526
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  2. ^
    PMID 24853682
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  3. S2CID 1096295
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  4. PMID 10764638
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  5. PMID 31447178
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  6. doi:10.1101/2019.12.26.888982
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  8. PMID 24445575
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  9. PMID 23734637
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  10. PMID 27293326
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  11. S2CID 24156261
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  12. PMID 16362644
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  13. ^ Schön and Boehncke, Psoriasis: Neurogenic inflammation and other mechanisms NEJM 352:1899-1912, Number 18, 2005
  14. ^
    S2CID 9257957
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  15. PMID 11829413
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  16. S2CID 24135943
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  17. ^ Meggs, William J. The Role of Neurogenic Inflammation in Chemical Sensitivity (2017) EcopsychologyVol. 9, No. 2 Published Online:1 Jun 2017 https://doi.org/10.1089/eco.2016.0045
  18. S2CID 28255407
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  19. PMID 9167992
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  20. PMID 18488069
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  21. PMID 18217201
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  22. PMID 11410074
    . Retrieved 14 June 2015.
  23. PMID 1384353
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  24. S2CID 43556609
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  25. ^ "UpToDate".
  26. ^ The Race to Offer CGRP for Migraine Migraine.com Editorial Team July 21, 2017
  27. PMID 6055248
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  28. PMID 20433208
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  29. S2CID 207195138
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  30. S2CID 26070466
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  31. ^ Clinical trial number NCT00816517 for "Use of Botulinum Toxin to Treat Psoriasis" at ClinicalTrials.gov
  32. ^ Product Information: Astelin, azelastine. Wallace Laboratories, Cranbury, NJ. (PI Revised 08/2000) PI Reviewed 01/2001
  33. S2CID 23292869
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  34. S2CID 1001915
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  35. PMID 22837035
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  36. PMID 22837035
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External links
Retrieved from "https://en.wikipedia.org/w/index.php?title=Neurogenic_inflammation&oldid=1218369249"