Reduced adrenal response to bacterial lipopolysaccharide in interleukin-6-deficient mice

Autor: F. H. J. Van Enckevort, C. C. Hermsen, Paul N. Span, Ad R. M. M. Hermus, Pierre N.M. Demacker, C.G.J. Sweep
Rok vydání: 2001
Předmět:
Lipopolysaccharides
Male
medicine.medical_specialty
Lipopolysaccharide
Endocrinology
Diabetes and Metabolism
medicine.medical_treatment
Sialoglycoproteins
gastheer-parasiet interactie [Malaria]
Stimulation
Adrenocorticotropic hormone
parasite-host interaction [Malaria]
Lipoproteïnen en atherosclerose
Biology
chemistry.chemical_compound
Mice
Endocrinology
Corticosterone
De rol van cytokinen in de pathofysiologie van koortsende ziekten en in de afweer tegen infecties
Internal medicine
Adrenal Glands
medicine
Animals
Humans
Interleukin 6
Chemical Endocrinology
Mice
Knockout
Lipoproteins and atherosclerose
Interleukin-6
Tumor Necrosis Factor-alpha
The role of cytokines in the pathophysiology of febrile illnesses and in host defense against infections
Interleukin
Antibodies
Monoclonal
Recombinant Proteins
Interleukin 1 Receptor Antagonist Protein
Cytokine
chemistry
biology.protein
Cytokines
Tumor necrosis factor alpha
Interleukin-1
Zdroj: Journal of Endocrinological Investigation, 24, 786--95
Journal of Endocrinological Investigation, 24, 10, pp. 786--95
ISSN: 1720-8386
Popis: Item does not contain fulltext Administration of bacterial lipopolysaccharide (LPS) in rodents induces the release of pro-inflammatory cytokines [tumor necrosis factor (TNF), interleukin (IL)-1, IL-6] and of ACTH and corticosterone. IL-6 is probably an important cytokine in the interaction between the immune system and the hypothalamus-pituitary-adrenal (HPA) axis, but so far the role of IL-6 in lipopolysaccharide (LPS)-induced HPA activation has not been established unequivocally. We examined the effects of intraperitoneal administration of LPS (range 0.25-2000 pg/mouse) on plasma corticosterone, TNFalpha and IL-1alpha levels in IL-6-deficient (IL-6 -/-) and wildtype control (IL-6 +/+) mice. Plasma corticosterone levels increased within one hour in both mouse strains. The corticosterone response was significantly reduced in IL-6 -/- mice, but no differences in TNFalpha or in IL-1alpha plasma levels were found between the two strains. Next, we studied the involvement of IL-1alpha or TNFalpha in the responses to LPS in IL-6 -/- and IL-6 +/+ mice by infusion of recombinant human IL-1 receptor antagonist (IL-1ra), or by injection of anti-TNFalpha antibodies. Pretreatment with IL-1ra or with anti-TNFalpha did not affect the corticosterone response to LPS, neither in IL-6 -/-, nor in IL-6 +/+ mice. Our data suggest that in the stimulation of the HPA axis by LPS in mice blockade of either IL-1alpha or TNFalpha may be compensated for by other mediators. The reduced adrenal response after LPS administration found in IL-6 -/- mice indicates a distinct role for IL-6 in the activation of the HPA axis by LPS.
Databáze: OpenAIRE
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