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1 Exp Physiol 6:339-354(1913). William J. Maggs divides his tirna between the Department of 3. Tanaka DT. Grunstein MM. Vasoactive Emergency Medicine at East Carolina University, where he is an effects of substance P on isolated rabbit pul­ assistant professor, and Bellevue Hospital Center, New York monary artery. J AppI Physiol 58:1291(1985). University, where he is a fellow in clinical toxicology. He received his 4. Foreman JC. Peptides and neurogenic inflam- mation. Br Med Bull 43:386( 1987). MO degree from the University of Miami and completed and internal medicine residency at the University of Rochester. Dr. Meggs is ; 5. Lundberg JM. Lundbiad L. Warding CR. Saha A. Stjamc P. Anggard A. Coexistence of multi­ board certified in intemal medicine, emergency medicine, and allergy ple peptides and classic traiumitrers in airway and clinical immunology. He is currently involved in research in . ncurotu. Am Rev Respir Dis 136:16(1987), toxin-induced asthma and rhinitis, chemical sensitivity syndromes, ' 6. Uddman R. Grunditz T, Larsson A. Sundlet F. and other areas of clinical toxicology. Dr. Meggs served on the Sensory innervation of rhe eat drum and mid­ immunotoxicology subcommittee of the National Academy of ; dle ear mucosa. Cell Tissue Res 252:141 Sciences, which authored the book Biologic Markers oflmmunotoidcologY. ■ (1988). 7. Hinsey JC and Gasset HS. The component of the dorsal root mediating vasodilatation and the Sherrington contracture. Am J Physiol Both the mediators and regulators of by environmental chemicals such as ciga­ 92:679(1930). inflammation may be released from the site rette smoke and solvents. Hence, any dis­ 8. Jancso-Gabor, A., Szolcsany J. Action of tare of inflammation and affect distant sites. order mediated by neurogenic inflamma­ earth metal complexes on neurogenic as well as tion can potentially be exacerbated by on bradykinin induced inflammation. ] Fhann Two important regulators of inflamma­ Pharmacol 22:366:135(1970). tion, interleukin 1 and interleukin 2, sup- environmental chemicals. Study of the 9. Gasparovic I, Hadzovic S. Hukovic S. Stem P. rcss central nervous system activity hypothesis that chemical sensitivity syn­ Contribution to the theory that substance P [50,51}. Another possibility is that some dromes such as SBS and MCS may result has a transmitter role in sensitive pathways. form of neural switching may take place. from neurogenic inflammation arising Med Exp 10:155-159(1964). That is, triggering of chemical irritant from stimulation of irritant receptors by 10. Gaielius B, Brodin E, Olgatt L, Panopoulos P. environmental chemicals may lead to an Evidence that substance P is a mediator of receptors in one organ could lead to an antidromic vasodilatation using somatostatin as efferent signal traveling to another site understanding of these disorden. It is of a release inhibitor. Acta Physiol Scand 113: through an aberrant or conditioned cross­ interest that the symptoms of headache, 155-159(1981). ing of the pathways. A combination of myalgia, arthralgias and arthritis, and air­ ll.ChahlLA. Antidromic vasodilatation and neu­ these two mechanisms may be operative. way symptoms reported by MCS patients rogenic inflammation. Pharmacol Ther 37: The hypothesis that neurogenic inflam­ overlap with those disorders for which a 275-300(1988). role for neurogenic inflammation has been 12. Ehrlanger J, Glasser HJ. The action potential mation is the mechanism of chemical sen­ in Abets of slow conduction in spinal roots and sitivity syndromes is amenable to scientific reported. somatic nerves. Ara J Physiol 90:338-339 study. Biopsies of the airways of chemical­ The hypothesis that neurogenic inflam­ (1929). ly sensitive individuals should be abnor­ mation triggered by environmental chemi­ 13. Nadel JA. Neutral endopeptidase modulates mal, with signs of inflammation. Im- cals plays a role in human health is amen­ neurogenic inflammation. Eur Respir J 4: munofluorescent monoclonal antibodies able to scientific study. Research should 745-754(1991). 14. Nielsen GD. Mechanisms of activation of the could be used to detect NEP, which focus on noninvasivc methods for detect­ sensory irritant receptor by airborne chemicals. should be decreased, and substance P, ing biomarkers of neurogenic inflamma­ Crit Rev Toxicol 21:183-208(1991). which should be elevated relative to con­ tion. Are there degradation products of 15. Comeno-Muniz JE. Cain WS. Thresholds for trols. Nasal washings should contain substance P or other mediators of neuro­ odor and nasal pungency. Physiol Behav increased levels of the mediators of neuro­ genic inflammation that are elevated in the 48:719-725(990). genic inflammation relative to controls, urine or serum of patients with activation 16. Lundblad L Protective reflexes and vascular of this system? Are there evoked potentials effects in the nasal mucosa elicited by activa­ and the levels should increase after chemi­ tion of capsaicin-sensitive substance P im­ cal challenge in patients but not controls. or nerve conduction parameters that can munoreactive trigeminal neurons. Acta Physiol Heightened neuronal firing of sensory be used to detect activation of neurogenic Scand 529(suppl) (1984). fibers should occur after chemical chal­ inflammation? Two groups of patients 17. Lundberg JM, Lundbblad L, Satia A. Angaard lenges. should be studied with challenge tests: A. Inhibition of cigarette smoke-induced oede­ patients with disorders in which neuro­ ma in the nasal mucosa by capsaicin pretreat­ Discussion genic inflammation is suspected to play a ment and a substance P antagonist. Naunyn- Schmiedebergs Arch Pharmakoi 326: 181 Neurogenic inflammation leads to inflam­ role (i.e., asthma, rhinitis, migraine, (1984). nation independent of the immune sys­ rheumatoid arthritis, fibromyalgia) and 18. Kohrogi H. Nadel JA. Malfroy B, Garman C, tem. Polypeptide mediators are stored in patients with chemical sensitivity syn­ Bridenbaugh R. Patton JS, Borson DB. nerve endings and released when irritant dromes. These patients should be isolated Recombinant human enkephalinase (neutral receptors on nerves are stimulated by from VOCs in a specially constructed clin­ endopeptidase) prevents cough induced by tachykinins in awake guinea pigs. J Clin Invest chemicals. The role of neurogenic inflam­ ical researc.*) unit and monitored for reso­ 84:781-786(1989). mation in a number of inflammatory con­ lution of their symptoms. Chemical chal- 19. Iwamoto 1. Ueki IF, Borson DB, Nadel JA. ditions is currently under investigation. . Icnges should be conducted while patients Neutral endopeptidase modulates tachykinin- There is strong evidence that neurogenic are monitored for provoked symptoms. induced increase in vascular permeability in inflammation is operative in asthma and Biomarkers of neurogenic inflammation guinea pig skin. Int Arch Allergy AppI Im­ rhinitis.- There is circumstantial evidence should be measured throughout the course munol 88:288-293(1989). of these challenges. 20. Rubenstein I, Iwamoto I, Ueki IF, Borson DB, hat neurogenic inflammation may play a Nadel JA. Recombinant neutral endopeptidase ole in migraine headache. Evidence for a attenuates substance P induced plasma extrava­ role in rheumatoid arthritis and fibromyal­ References sation in the guinea pig skin. Int Arch Allergy gia is not as compelling at this time. The 1. Bruce AN. Uber die Beziehung det Seiuiblen AppI Immunol 91:232-238(1990). significance of these associations for envi­ Nervenendigungen zura Enzundungtvorgang. 21. Dusse DJ, Djokic TD, Botson DB. Nadel JA. ronmental health is that neurogenic in­ Cigarette smoke induces bronchocoiutrictor Arch Exp Pathol Pharmakoi 63:424(1910). hyperresponsivencss in substance P and inacti- flammation can be triggered in the airways 2. Bruce AN. Vasodilatory axon reflexes. Q J

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