Suppression of in vitro antibody production by corticotropin-releasing factor neurohormone

Sye Jye Christine Leu, Vijendra K. Singh

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Corticotropin-releasing factor (CRF) is a peptide hormone that regulates the synthesis of pro-opiomelanocortin (POMC)-derived bioactive peptides from the cells of both neuroendocrine system and immune system. In this study, the effect of CRF on in vitro production of antibodies was investigated. The peripheral blood mononuclear cells (MNC), at a concentration of 1 × 106 cells ml-1, from several healthy blood donors were stimulated to produce immunoglobulins with 25 μg ml-1 pokeweed mitogen (PWM) in the presence of different concentrations of CRF (10-16 to 10-7 M range). After 7 days of incubation, the cell cultures were centrifuged, and the supernatants quantified for IgG, IgM, and IgA by enzyme-linked immunosorbent assay (ELISA). At concentrations of 10-13 M or greater, the CRF and three structurally related peptides (Tyr-CRF, α-helical CRF9-41, and sauvagine) caused a statistically significant (P <0.001) suppression of the production of all three isotypes of Ig. At a antagonist: agonist ratio of as high as 100:1, the antagonist α-helical CRF9-41 did not antagonize the inhibitory action of CRF, instead it showed synergism with CRF by accentuating the CRF-induced suppression of IgG synthesis. This unexpected result may be due to the involvement of a subtype of CRF receptor which is insensitive to α-helical CRF. Moreover, the production of all three Ig isotypes was suppressed by rabbit antihuman-interleukin-1 (anti-IL-1) or rabbit antihuman-β-endorphin (anti-βE) or monocyte-depeletion, but neither treatment significantly modified the CRF-induced suppression of antibody production. These indirect studies suggest that the B cell response factors other than the IL-1 and βE may be involved in the mechanism of action of CRF-induced suppression of PWM-stimulated antibody production by human MNC.

Original languageEnglish
Pages (from-to)23-29
Number of pages7
JournalJournal of Neuroimmunology
Volume45
Issue number1-2
DOIs
Publication statusPublished - 1993
Externally publishedYes

Fingerprint

Corticotropin-Releasing Hormone
Antibody Formation
Neurotransmitter Agents
Pokeweed Mitogens
Interleukin-1
In Vitro Techniques
Immunoglobulin G
Rabbits
Endorphins
Corticotropin-Releasing Hormone Receptors
Pro-Opiomelanocortin
Peptides
Neurosecretory Systems
Peptide Hormones
Blood Donors
Immunoglobulin A
Immunoglobulin M
Immunoglobulins
Monocytes
Immune System

Keywords

  • Corticotropin-releasing factor
  • In vitro antibody production
  • Neuroendocrine-immune axis
  • Stress-induced immunosuppression

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy
  • Clinical Neurology
  • Neurology

Cite this

Suppression of in vitro antibody production by corticotropin-releasing factor neurohormone. / Leu, Sye Jye Christine; Singh, Vijendra K.

In: Journal of Neuroimmunology, Vol. 45, No. 1-2, 1993, p. 23-29.

Research output: Contribution to journalArticle

@article{51312811e56b4c1eb0fd450aaf59fdf0,
title = "Suppression of in vitro antibody production by corticotropin-releasing factor neurohormone",
abstract = "Corticotropin-releasing factor (CRF) is a peptide hormone that regulates the synthesis of pro-opiomelanocortin (POMC)-derived bioactive peptides from the cells of both neuroendocrine system and immune system. In this study, the effect of CRF on in vitro production of antibodies was investigated. The peripheral blood mononuclear cells (MNC), at a concentration of 1 × 106 cells ml-1, from several healthy blood donors were stimulated to produce immunoglobulins with 25 μg ml-1 pokeweed mitogen (PWM) in the presence of different concentrations of CRF (10-16 to 10-7 M range). After 7 days of incubation, the cell cultures were centrifuged, and the supernatants quantified for IgG, IgM, and IgA by enzyme-linked immunosorbent assay (ELISA). At concentrations of 10-13 M or greater, the CRF and three structurally related peptides (Tyr-CRF, α-helical CRF9-41, and sauvagine) caused a statistically significant (P <0.001) suppression of the production of all three isotypes of Ig. At a antagonist: agonist ratio of as high as 100:1, the antagonist α-helical CRF9-41 did not antagonize the inhibitory action of CRF, instead it showed synergism with CRF by accentuating the CRF-induced suppression of IgG synthesis. This unexpected result may be due to the involvement of a subtype of CRF receptor which is insensitive to α-helical CRF. Moreover, the production of all three Ig isotypes was suppressed by rabbit antihuman-interleukin-1 (anti-IL-1) or rabbit antihuman-β-endorphin (anti-βE) or monocyte-depeletion, but neither treatment significantly modified the CRF-induced suppression of antibody production. These indirect studies suggest that the B cell response factors other than the IL-1 and βE may be involved in the mechanism of action of CRF-induced suppression of PWM-stimulated antibody production by human MNC.",
keywords = "Corticotropin-releasing factor, In vitro antibody production, Neuroendocrine-immune axis, Stress-induced immunosuppression",
author = "Leu, {Sye Jye Christine} and Singh, {Vijendra K.}",
year = "1993",
doi = "10.1016/0165-5728(93)90159-V",
language = "English",
volume = "45",
pages = "23--29",
journal = "Journal of Neuroimmunology",
issn = "0165-5728",
publisher = "Elsevier",
number = "1-2",

}

TY - JOUR

T1 - Suppression of in vitro antibody production by corticotropin-releasing factor neurohormone

AU - Leu, Sye Jye Christine

AU - Singh, Vijendra K.

PY - 1993

Y1 - 1993

N2 - Corticotropin-releasing factor (CRF) is a peptide hormone that regulates the synthesis of pro-opiomelanocortin (POMC)-derived bioactive peptides from the cells of both neuroendocrine system and immune system. In this study, the effect of CRF on in vitro production of antibodies was investigated. The peripheral blood mononuclear cells (MNC), at a concentration of 1 × 106 cells ml-1, from several healthy blood donors were stimulated to produce immunoglobulins with 25 μg ml-1 pokeweed mitogen (PWM) in the presence of different concentrations of CRF (10-16 to 10-7 M range). After 7 days of incubation, the cell cultures were centrifuged, and the supernatants quantified for IgG, IgM, and IgA by enzyme-linked immunosorbent assay (ELISA). At concentrations of 10-13 M or greater, the CRF and three structurally related peptides (Tyr-CRF, α-helical CRF9-41, and sauvagine) caused a statistically significant (P <0.001) suppression of the production of all three isotypes of Ig. At a antagonist: agonist ratio of as high as 100:1, the antagonist α-helical CRF9-41 did not antagonize the inhibitory action of CRF, instead it showed synergism with CRF by accentuating the CRF-induced suppression of IgG synthesis. This unexpected result may be due to the involvement of a subtype of CRF receptor which is insensitive to α-helical CRF. Moreover, the production of all three Ig isotypes was suppressed by rabbit antihuman-interleukin-1 (anti-IL-1) or rabbit antihuman-β-endorphin (anti-βE) or monocyte-depeletion, but neither treatment significantly modified the CRF-induced suppression of antibody production. These indirect studies suggest that the B cell response factors other than the IL-1 and βE may be involved in the mechanism of action of CRF-induced suppression of PWM-stimulated antibody production by human MNC.

AB - Corticotropin-releasing factor (CRF) is a peptide hormone that regulates the synthesis of pro-opiomelanocortin (POMC)-derived bioactive peptides from the cells of both neuroendocrine system and immune system. In this study, the effect of CRF on in vitro production of antibodies was investigated. The peripheral blood mononuclear cells (MNC), at a concentration of 1 × 106 cells ml-1, from several healthy blood donors were stimulated to produce immunoglobulins with 25 μg ml-1 pokeweed mitogen (PWM) in the presence of different concentrations of CRF (10-16 to 10-7 M range). After 7 days of incubation, the cell cultures were centrifuged, and the supernatants quantified for IgG, IgM, and IgA by enzyme-linked immunosorbent assay (ELISA). At concentrations of 10-13 M or greater, the CRF and three structurally related peptides (Tyr-CRF, α-helical CRF9-41, and sauvagine) caused a statistically significant (P <0.001) suppression of the production of all three isotypes of Ig. At a antagonist: agonist ratio of as high as 100:1, the antagonist α-helical CRF9-41 did not antagonize the inhibitory action of CRF, instead it showed synergism with CRF by accentuating the CRF-induced suppression of IgG synthesis. This unexpected result may be due to the involvement of a subtype of CRF receptor which is insensitive to α-helical CRF. Moreover, the production of all three Ig isotypes was suppressed by rabbit antihuman-interleukin-1 (anti-IL-1) or rabbit antihuman-β-endorphin (anti-βE) or monocyte-depeletion, but neither treatment significantly modified the CRF-induced suppression of antibody production. These indirect studies suggest that the B cell response factors other than the IL-1 and βE may be involved in the mechanism of action of CRF-induced suppression of PWM-stimulated antibody production by human MNC.

KW - Corticotropin-releasing factor

KW - In vitro antibody production

KW - Neuroendocrine-immune axis

KW - Stress-induced immunosuppression

UR - http://www.scopus.com/inward/record.url?scp=0027162113&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027162113&partnerID=8YFLogxK

U2 - 10.1016/0165-5728(93)90159-V

DO - 10.1016/0165-5728(93)90159-V

M3 - Article

VL - 45

SP - 23

EP - 29

JO - Journal of Neuroimmunology

JF - Journal of Neuroimmunology

SN - 0165-5728

IS - 1-2

ER -