Medicine:Neurogenic inflammation

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Neurogenic inflammation is inflammation arising from the local release by afferent neurons of inflammatory mediators such as Substance P, Calcitonin Gene-Related Peptide (CGRP), neurokinin A (NKA), and 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 pathogenesis of numerous diseases including migraine,[10][1][11][12] psoriasis,[2][13][14] asthma,[15] vasomotor rhinitis,[16] fibromyalgia, eczema, rosacea, dystonia, and multiple chemical sensitivity. [17][18][19]

In migraine, stimulation of the trigeminal nerve causes neurogenic inflammation via release of neuropeptides including Substance P, nitric oxide, vasoactive intestinal polypeptide, 5-HT, Neurokinin A and CGRP.[20][21] leading to a "sterile neurogenic inflammation."[22]

Prevention

Magnesium deficiency causes neurogenic inflammation in a rat model. Researchers have theorized that since substance P which appears at day five of induced magnesium deficiency, is known to stimulate in turn the production of other inflammatory cytokines including IL-1, Interleukin 6 (IL-6), and TNF-alpha (TNFα), which begin a sharp rise at day 12, substance P is a key in the path from magnesium deficiency to the subsequent cascade of neuro-inflammation.[23] In a later study, researchers provided rats dietary levels of magnesium that were reduced but still within the range of dietary intake found in the human population, and observed an increase in substance P, TNF alpha (TNFα) and 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 (Azelastine) "is indicated for symptomatic treatment of 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. ↑ 1.0 1.1 "Neurogenic inflammation and migraine: implications for the therapeutics". Mol. Interv. 5 (5): 304–11. October 2005. doi:10.1124/mi.5.5.10. PMID 16249526. 
  2. ↑ 2.0 2.1 "Brain-skin connection: stress, inflammation and skin aging". Inflamm Allergy Drug Targets 13 (3): 177–90. 2014. doi:10.2174/1871528113666140522104422. PMID 24853682. 
  3. ↑ "The concept of neurogenic inflammation". BJU Int. 101 (Suppl 3): 2–6. March 2008. doi:10.1111/j.1464-410X.2008.07493.x. PMID 18307678. 
  4. ↑ Caterina, M. J.; Leffler, A.; Malmberg, A. B.; Martin, W. J.; Trafton, J.; Petersen-Zeitz, K. R.; Koltzenburg, M.; Basbaum, A. I. et al. (2000-04-14). "Impaired nociception and pain sensation in mice lacking the capsaicin receptor". Science 288 (5464): 306–313. doi:10.1126/science.288.5464.306. ISSN 0036-8075. PMID 10764638. Bibcode: 2000Sci...288..306C. 
  5. ↑ Lin King, John V.; Emrick, Joshua J.; Kelly, Mark J. S.; Herzig, Volker; King, Glenn F.; Medzihradszky, Katalin F.; Julius, David (2019-09-05). "A Cell-Penetrating Scorpion Toxin Enables Mode-Specific Modulation of TRPA1 and Pain". Cell 178 (6): 1362–1374.e16. doi:10.1016/j.cell.2019.07.014. ISSN 1097-4172. PMID 31447178. 
  6. ↑ Zhao, Jianhua; King, John V. Lin; Cheng, Yifan; Julius, David (2019-12-27). "Mechanisms governing irritant-evoked activation and calcium modulation of TRPA1" (in en). bioRxiv: 2019.12.26.888982. doi:10.1101/2019.12.26.888982. https://www.biorxiv.org/content/10.1101/2019.12.26.888982v1. 
  7. ↑ Zhao, Jianhua; Lin King, John V.; Paulsen, Candice E.; Cheng, Yifan; Julius, David (2020-07-08). "Irritant-evoked activation and calcium modulation of the TRPA1 receptor" (in en). Nature 585 (7823): 141–145. doi:10.1038/s41586-020-2480-9. ISSN 0028-0836. PMID 32641835. Bibcode: 2020Natur.585..141Z. 
  8. ↑ "TRPA1 channels mediate acute neurogenic inflammation and pain produced by bacterial endotoxins". Nat Commun 5: 3125. 2014. doi:10.1038/ncomms4125. PMID 24445575. Bibcode: 2014NatCo...5.3125M. 
  9. ↑ "The role of histamine in neurogenic inflammation". Br. J. Pharmacol. 170 (1): 38–45. September 2013. doi:10.1111/bph.12266. PMID 23734637. 
  10. ↑ "Understanding migraine: Potential role of neurogenic inflammation". Ann Indian Acad Neurol 19 (2): 175–82. 2016. doi:10.4103/0972-2327.182302. PMID 27293326. 
  11. ↑ "Peripheral mechanism of action of antimigraine prophylactic drugs". Neurol. Sci. 29 (Suppl 1): S127–30. May 2008. doi:10.1007/s10072-008-0903-8. PMID 18545913. 
  12. ↑ "CGRP and migraine: neurogenic inflammation revisited". J Headache Pain 6 (2): 61–70. April 2005. doi:10.1007/s10194-005-0153-6. PMID 16362644. 
  13. ↑ Schön and Boehncke, Psoriasis: Neurogenic inflammation and other mechanisms NEJM 352:1899-1912, Number 18, 2005
  14. ↑ 14.0 14.1 "The role of neuropeptides in psoriasis". Br. J. Dermatol. 155 (5): 876–82. November 2006. doi:10.1111/j.1365-2133.2006.07518.x. PMID 17034513. 
  15. ↑ "Neurogenic inflammation and particulate matter (PM) air pollutants". Neurotoxicology 22 (6): 795–810. December 2001. doi:10.1016/S0161-813X(01)00062-6. PMID 11829413. https://zenodo.org/record/1259847. 
  16. ↑ "[Ultrastructural changes in allergic rhinitis vs. idiopathic rhinitis]" (in de). HNO 56 (8): 799–807. August 2008. doi:10.1007/s00106-008-1764-4. PMID 18651116. 
  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. ↑ "Brain dysfunction in multiple chemical sensitivity". J. Neurol. Sci. 287 (1–2): 72–8. December 2009. doi:10.1016/j.jns.2009.09.003. PMID 19801154. 
  19. ↑ "Neurogenic inflammation: with additional discussion of central and perceptual integration of nonneurogenic inflammation". Environ. Health Perspect. 105 (Suppl 2): 531–7. March 1997. doi:10.1289/ehp.97105s2531. PMID 9167992. 
  20. ↑ "Acute migraine: Current treatment and emerging therapies". Ther Clin Risk Manag 3 (3): 449–59. June 2007. PMID 18488069. 
  21. ↑ "Treatment of migraine attacks based on the interaction with the trigemino-cerebrovascular system". J Headache Pain 9 (1): 5–12. February 2008. doi:10.1007/s10194-008-0011-4. PMID 18217201. 
  22. ↑ Grossmann, MD, Werner; Schmidramsl, MD, Hanns (2001). "An Extract of Petasites hybridus Is Effective in the Prophylaxis of Migraine". Alternative Medicine Review 6 (3): 303–10. PMID 11410074. http://www.altmedrev.com/publications/6/3/303.pdf. Retrieved 14 June 2015. 
  23. ↑ "Pathobiology of magnesium deficiency: a cytokine/neurogenic inflammation hypothesis". Am. J. Physiol. 263 (3 Pt 2): R734–7. September 1992. doi:10.1152/ajpregu.1992.263.3.R734. PMID 1384353. 
  24. ↑ "Skeletal and hormonal effects of magnesium deficiency". J Am Coll Nutr 28 (2): 131–41. April 2009. doi:10.1080/07315724.2009.10719764. PMID 19828898. 
  25. ↑ "UpToDate". https://www.uptodate.com/contents/preventive-treatment-of-migraine-in-adults?search=migraine%20treatment&sectionRank=1&usage_type=default&anchor=H382445576&source=machineLearning&selectedTitle=2~150&display_rank=2#H382445576. 
  26. ↑ The Race to Offer CGRP for Migraine Migraine.com Editorial Team July 21, 2017
  27. ↑ "Direct evidence for neurogenic inflammation and its prevention by denervation and by pretreatment with capsaicin". Br J Pharmacol Chemother 31 (1): 138–51. September 1967. doi:10.1111/j.1476-5381.1967.tb01984.x. PMID 6055248. 
  28. ↑ "Calcitonin gene-related peptide (CGRP) receptor antagonists in the treatment of migraine". CNS Drugs 24 (7): 539–48. July 2010. doi:10.2165/11534920-000000000-00000. PMID 20433208. 
  29. ↑ "Proinflammatory mediators and migraine pathogenesis: moving towards CGRP as a target for a novel therapeutic class". Expert Rev Neurother 8 (9): 1347–54. September 2008. doi:10.1586/14737175.8.9.1347. PMID 18759547. 
  30. ↑ "Future drugs for migraine". Intern Emerg Med 4 (5): 367–73. October 2009. doi:10.1007/s11739-009-0273-0. PMID 19551474. 
  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. ↑ "Vasomotor rhinitis: clinical efficacy of azelastine nasal spray in comparison with placebo". ORL J. Otorhinolaryngol. Relat. Spec. 63 (2): 76–81. 2001. doi:10.1159/000055714. PMID 11244365. 
  34. ↑ "Statins decrease expression of the proinflammatory neuropeptides calcitonin gene-related peptide and substance P in sensory neurons". J. Pharmacol. Exp. Ther. 324 (3): 1172–80. March 2008. doi:10.1124/jpet.107.132795. PMID 18079356. 
  35. ↑ "Neurogenic inflammation and the peripheral nervous system in host defense and immunopathology". Nat. Neurosci. 15 (8): 1063–7. July 2012. doi:10.1038/nn.3144. PMID 22837035. 
  36. ↑ "Neurogenic inflammation and the peripheral nervous system in host defense and immunopathology". Nat Neurosci 15 (8): Figure 3. 2012. doi:10.1038/nn.3144. PMID 22837035. 

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