Toll-like receptor 9 expression in murine and human adrenal glands and possible implications during inflammation.
J Clin Endocrinol Metab
; 92(7): 2773-83, 2007 Jul.
Article
em En
| MEDLINE
| ID: mdl-17473064
ABSTRACT
CONTEXT Sepsis is a leading cause of death in the Western world and can be associated with failure of the hypothalamic-pituitary-adrenal axis. A coordinated response of the adrenal and immune system is of vital importance for survival during sepsis. Within the immune response, Toll-like receptors (TLRs) play a crucial role by recognizing pathogen-associated molecules such as bacterial DNA. TLR-9 can detect motifs of unmethylated cytosine-phosphate-guanine (CpG) dinucleotides (CpG-DNA) being present in bacterial DNA. OBJECTIVE:
We investigated whether TLR-9 is expressed in human and murine adrenal glands and whether its activation is associated with an adrenal response.DESIGN:
Human fetal and adult adrenal glands; wild-type, C57BL/6 and TLR-9 deficient (TLR-9-/-) mice; and in vitro cell line models were used in the study.SETTING:
The study took place at a university hospital.RESULTS:
TLR-9 is expressed in human and murine adrenal glands, as well as in in vitro cell lines (Y-1 and NCI-H295R cells). CpG-oligodeoxynucleotide challenge caused a 3-fold increase in plasma levels of corticosterone in wild-type mice. This effect was not observed in TLR-9-/- mice. Furthermore, CpG-oligodeoxynucleotide challenge resulted in a strong release of several inflammatory cytokines, such as TNF-alpha, and IL-1beta, -6, -10, and -12 in vivo as well as in vitro. Again, this effect was not present in TLR-9-/- mice.CONCLUSIONS:
TLR-9 is present in both murine and human adrenal glands. TLR-9 stimulation led to a corticosterone and inflammatory cytokine response. TLR-9 may play a role in the regulation of the hypothalamic-pituitary-adrenal axis during conditions in which bacterial DNA is present.
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Base de dados:
MEDLINE
Assunto principal:
Córtex Suprarrenal
/
Sepse
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Receptor Toll-Like 9
Idioma:
En
Ano de publicação:
2007
Tipo de documento:
Article
País de afiliação:
Reino Unido