The JI
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     
 


This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Warwick-Davies, J.
Right arrow Articles by Cole, P. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Warwick-Davies, J.
Right arrow Articles by Cole, P. J.

The Journal of Immunology, Vol 154, Issue 4 1909-1918, Copyright © 1995 by American Association of Immunologists


ARTICLES

Growth hormone is a human macrophage activating factor. Priming of human monocytes for enhanced release of H2O2

J Warwick-Davies, DB Lowrie and PJ Cole
Host Defense Unit, Royal Brompton National Heart and Lung Institute, London, United Kingdom.

Although many effects of growth hormone (GH) and related factors upon the immune system have been demonstrated, few studies have examined the capacity of these factors to modulate human monocyte function in vitro. Assaying a range of mediators, only GH and prolactin (PRL), at 0.3 to 1.0 micrograms/ml, and growth hormone-releasing hormone (GRH) at very high doses, primed monocytes for enhanced hydrogen-peroxide production (H2O2) in response to PMA. GH-induced priming was not caused by endotoxin, nor by production of lymphokines such as IFN-gamma. Exogenous insulin-like growth factor-I (IGF-I), alone or in combination with GH, was without effect, making it unlikely that GH mediates its effects on monocytes via an autocrine/paracrine action of IGF-I. Monocytes specifically bound radiolabeled GH and contained mRNA for the GH receptor and, in some donors, the PRL receptor. Therefore, GH probably exerts its effects as a human macrophage-activating factor through either GH or PRL receptors, without requiring production of IGF- I.


This article has been cited by other articles:


Home page
Eur Respir JHome page
C. Grasemann, F. Ratjen, D. Schnabel, E. Reutershahn, U. Vester, and H. Grasemann
Effect of growth hormone therapy on nitric oxide formation in cystic fibrosis patients
Eur. Respir. J., April 1, 2008; 31(4): 815 - 821.
[Abstract] [Full Text] [PDF]


Home page
Infect. Immun.Home page
R. Campos-Rodriguez, A. Quintanar-Stephano, R. A. Jarillo-Luna, G. Oliver-Aguillon, J. Ventura-Juarez, V. Rivera-Aguilar, I. Berczi, and K. Kovacs
Hypophysectomy and Neurointermediate Pituitary Lobectomy Reduce Serum Immunoglobulin M (IgM) and IgG and Intestinal IgA Responses to Salmonella enterica Serovar Typhimurium Infection in Rats
Infect. Immun., March 1, 2006; 74(3): 1883 - 1889.
[Abstract] [Full Text] [PDF]


Home page
Eur J EndocrinolHome page
S. Pagani, C. Meazza, P. Travaglino, F. De Benedetti, C. Tinelli, and M. Bozzola
Serum cytokine levels in GH-deficient children during substitutive GH therapy
Eur. J. Endocrinol., February 1, 2005; 152(2): 207 - 210.
[Abstract] [Full Text] [PDF]


Home page
Annals of Clinical & Laboratory ScienceHome page
Z. Liu, Y. Yu, Y. Jiang, and J. Li
Growth Hormone Increases Lung NF-{kappa}B Activation and Lung Microvascular Injury Induced by Lipopolysaccharide in Rats
Ann. Clin. Lab. Sci., April 1, 2002; 32(2): 164 - 170.
[Abstract] [Full Text] [PDF]


Home page
J. Clin. Endocrinol. Metab.Home page
S. H. Zarkesh-Esfahani, O. Kolstad, R. A. Metcalfe, P. F. Watson, S. Von Laue, S. Walters, A. Revhaug, A. P. Weetman, and R. J. M. Ross
High-Dose Growth Hormone Does Not Affect Proinflammatory Cytokine (Tumor Necrosis Factor-{alpha}, Interleukin-6, and Interferon-{gamma}) Release from Activated Peripheral Blood Mononuclear Cells or after Minimal to Moderate Surgical Stress
J. Clin. Endocrinol. Metab., September 1, 2000; 85(9): 3383 - 3390.
[Abstract] [Full Text]


Home page
Endocr. Rev.Home page
K. Dorshkind and N. D. Horseman
The Roles of Prolactin, Growth Hormone, Insulin-Like Growth Factor-I, and Thyroid Hormones in Lymphocyte Development and Function: Insights from Genetic Models of Hormone and Hormone Receptor Deficiency
Endocr. Rev., June 1, 2000; 21(3): 292 - 312.
[Abstract] [Full Text]


Home page
NEJMHome page
J. Takala, E. Ruokonen, N. R. Webster, M. S. Nielsen, D. F. Zandstra, G. Vundelinckx, and C. J. Hinds
Increased Mortality Associated with Growth Hormone Treatment in Critically Ill Adults
N. Engl. J. Med., September 9, 1999; 341(11): 785 - 792.
[Abstract] [Full Text] [PDF]


Home page
EndocrinologyHome page
W. Liao, M. Rudling, and B. Angelin
Contrasting Effects of Growth Hormone and Insulin-Like Growth Factor I on the Biological Activities of Endotoxin in the Rat
Endocrinology, January 1, 1997; 138(1): 289 - 295.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1995 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1995 by The American Association of Immunologists, Inc. All rights reserved.