Immune deviation following stress odor exposure: role of endogenous opioids

Olfactory cues can alter immune function. BALB/c mice exposed to odors produced by footshock stressed donor mice have increased antibody responses and increased splenic interleukin (IL)-4 production following immunization relative to recipients of odors from unstressed animals. Here we document that...

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Bibliographic Details
Published in:Journal of neuroimmunology 2000-01, Vol.102 (2), p.145-153
Main Authors: Moynihan, Jan A, Karp, Jonathan D, Cohen, Nicholas, Ader, Robert
Format: Article
Language:English
Subjects:
Administration, Oral
Analgesia
Animals
Antibody
Antibody Formation - drug effects
Cells, Cultured
Endorphins - physiology
Hemocyanins - immunology
Immune System - physiology
Immunoglobulin G - drug effects
Immunoglobulin M - drug effects
Interleukin-4 - antagonists & inhibitors
Interleukin-4 - biosynthesis
Male
Mice
Mice, Inbred BALB C
naltrexone
Naltrexone - administration & dosage
Naltrexone - pharmacology
Narcotic Antagonists - administration & dosage
Narcotic Antagonists - pharmacology
Odorants
Opioids
Psychosocial stress
Spleen - cytology
Spleen - metabolism
Stress, Psychological - metabolism
Th2 cytokines
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Summary:Olfactory cues can alter immune function. BALB/c mice exposed to odors produced by footshock stressed donor mice have increased antibody responses and increased splenic interleukin (IL)-4 production following immunization relative to recipients of odors from unstressed animals. Here we document that exposure to stress odors results in analgesia that is blocked by the non-selective opioid receptor antagonist naltrexone. The stress odor-induced increase in antigen-driven IL-4 and antibody is also blocked by oral administration of naltrexone. Thus, we provide evidence that immune deviation can occur following a psychosocial stressor, and that the deviation appears to be mediated by endogenous opioid production.
ISSN:0165-5728
1872-8421
DOI:10.1016/S0165-5728(99)00173-3