Migration inhibitory factor expression in experimentally induced endotoxemia

Détails

ID Serval
serval:BIB_8C35B8B2F4F7
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Migration inhibitory factor expression in experimentally induced endotoxemia
Périodique
American Journal of Pathology
Auteur(s)
Bacher  M., Meinhardt  A., Lan  H. Y., Mu  W., Metz  C. N., Chesney  J. A., Calandra  T., Gemsa  D., Donnelly  T., Atkins  R. C., Bucala  R.
ISSN
0002-9440 (Print)
Statut éditorial
Publié
Date de publication
01/1997
Volume
150
Numéro
1
Pages
235-246
Notes
Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. --- Old month value: Jan
Résumé
Macrophage migration inhibitory factor (MIF) is an important constituent of the host response to stress and infection and is the first mediator that has been identified to be released from immune cells upon stimulation with glucocorticoids. MIF also has been shown to be secreted from the anterior pituitary gland, monocytes/macrophages, and T cells activated by various proinflammatory stimuli. Once released, MIF acts to counter-regulate the inhibitory effect of glucocorticoids on inflammatory cytokine production. To characterize more precisely the role of MIF in the host response to infection, we undertook a systematic analysis of MIF expression in various organs of the rat after endotoxin (lipopolysaccharide) administration. MIF protein and mRNA were analyzed by immunohistochemistry and in situ hybridization, respectively. MIF was found to be expressed constitutively in organs such as the lung, liver, kidney, spleen, adrenal gland, and skin. Significant quantities of MIF protein were detected preformed in various cell types and appeared to be released as a consequence of endotoxemia. In virtually all tissues examined, the loss of MIF protein 6 hours after lipopolysaccharide administration was accompanied by the induction of MIF mRNA and, at 24 hours, by the restoration of immunoreactive, intracellular MIF. The constitutive production of MIF by several cell and tissue types together with its rapid release from intracellular pools distinguishes MIF from other cytokines or hormonal mediators and significantly expands the physiological role of this unique counter-regulator of glucocorticoid action.
Mots-clé
Adrenal Glands/immunology/metabolism Animals Bone Marrow/immunology/metabolism Digestive System/immunology/metabolism Endotoxemia/chemically induced/*immunology/*metabolism Kidney/immunology/metabolism Liver/immunology/metabolism Lung/immunology/metabolism Macrophage Migration-Inhibitory Factors/*biosynthesis Male Rats Rats, Wistar Skin/immunology/metabolism Spleen/immunology/metabolism Thymus Gland/immunology/metabolism
Pubmed
Web of science
Création de la notice
25/01/2008 14:28
Dernière modification de la notice
03/03/2018 19:13
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