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Substance P-Mediated Modulation of the Primary Antibody Response

  • A. Eglezos
  • R. D. Helme
  • G. W. Dandie
  • P. V. Andrews
  • R. L. Boyd
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 237)

Abstract

The undecapeptide Substance P (SP) which is contained in primary afferent nerves, has been shown to affect certain components of the neurogenic inflammatory response including vasodilatation and plasma extravasation. Substance P also modulates the in vitro responses of lymphocytes and accessory cells. Rats treated neonatally with the sensory neurotoxin capsaicin, show a diminished neurogenic inflammatory response, but the effects of capsaicin treatment on cells of the immune system have not been previously documented. Using Sprague-Dawley rats at 6–12 weeks of age that had been pretreated neonatally with capsaicin, we examined the primary antibody response of popliteal lymph-node lymphocytes to antigenic stimulation in vivo with sheep red blood cells. It was observed that the number of cells secreting antigen-specific immunoglobulins was decreased in the capsaicin pretreated rat by more than 85%. This reduced response was reversed by a sub-cutaneous infusion of SP at the injection site immediately following antigenic stimulation. The results suggest that the decreased response in the capsaicin treated rats is secondary to the neurotoxic effects of capsaicin, and is most probably mediated by SP.

Keywords

Primary Afferent Nerve Popliteal Lymph Node Plasma Extravasation Capsaicin Treatment Primary Antibody Response 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. 1.
    N. Jansco, A. Jansco-Gabor, and J. Szolcsanyi, Br. J. Pharmacol. Chemoter. 312: 138 (1967).Google Scholar
  2. 2.
    W. M. Bayliss, J. Physiol. (Lond.) 26: 173 (1901).Google Scholar
  3. 3.
    J. I. Nagy, L. L. Iversen, M. Goedert, D. Chapman, and S. D. Hunt, J. Neurosci. 3: 399 (1983).PubMedGoogle Scholar
  4. 4.
    M. Fitzgerald, Pain 15: 109 (1983).PubMedCrossRefGoogle Scholar
  5. 5.
    D. G. Payan, D. R. Brewster, A. Missirian-Bastian, and E. J. Goetzl, J. Clin. Invest. 74: 1532 (1984).PubMedCrossRefGoogle Scholar
  6. 6.
    R. D. Helme and P. V. Andrews, J. Neurosci. Res. 13: 453 (1985).PubMedCrossRefGoogle Scholar
  7. 7.
    N. Jansco, A. Jansco-Gabor, and I. Takats, Acta Physiol. Acad. Sci. Hung. 19: 113 (1961).Google Scholar
  8. 8.
    A. J. Cunningham and A. Szenberg, Immunology 14: 599 (1968).PubMedGoogle Scholar
  9. 9.
    D. G. Payan, J. D. Levine, and E. J. Goetzl, J. Immunol. 132: 1601 (1984).PubMedGoogle Scholar
  10. 10.
    M. S. O’Dorisio, Fed. Proc. 46: 192 (1987).PubMedGoogle Scholar
  11. 11.
    R. D. Helme, A. Eglezos, and P. V. Andrews, Clin. Exp. Neurol. In press.Google Scholar
  12. 12.
    R. D. Helme, A. Eglezos, and C.S. Hosking, Immunol. Cell Biol. 65 (Pt.3): 267 (1987).PubMedCrossRefGoogle Scholar
  13. 13.
    A. M. Stanisz, D. Befus, and J. Bienenstock, J. Immunol. 136: 152 (1986).PubMedGoogle Scholar

Copyright information

© Plenum Press, New York 1988

Authors and Affiliations

  • A. Eglezos
    • 1
  • R. D. Helme
    • 2
  • G. W. Dandie
    • 1
  • P. V. Andrews
    • 2
  • R. L. Boyd
    • 1
  1. 1.Department of Pathology and Immunology, Alfred HospitalMonash UniversityAustralia
  2. 2.Department of Medicine, Prince Henry’s HospitalMonash UniversityMelbourneAustralia

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