The lack of glucocorticoid receptor on noradrenergic cells does not influence an inflammatory response after chronic stress

• Autorzy: Kusmierczyk J. , Chmielarz P. , Trojan E. , Roman A. , Nalepa I.
• Języki publikacji: EN

Abstrakty

EN

BACKGROUND AND AIMS: Noradrenergic neurons with terminals in the hypothalamus are known to regulate activity of the hypothalamic pituitary adrenal (HPA) axis. The aim of the study was to evaluate whether glucocorticoid receptor (GR) ablation in noradrenergic cells affects the inflammatory response in the central nervous system (CNS) and functioning of immune organs under chronic restraint stress (CIS) conditions. METHODS: Selective ablation of GRs in the noradrenergic system (GRDBHCre mice) was achieved using the Cre/loxP approach. The male mice were kept in standard laboratory conditions. The CIS procedure was performed by placing animals, for 2 hours daily, in 50 ml disposable centrifuge tubes and was repeated for 14 days The expression of cytokines in selected brain structure was analyzed with TaqMan RT-PCR assay. The relative thymus and spleen mass were calculated as well as peritoneal cell ability to production of selected cytokines after stimulation. RESULTS: We found that CIS procedure caused the decrease in body and relative thymus weights in both wt and mutant mice. The mRNA expression of interferon gamma and interleukin-6 genes was elevated in the hypothalamus, prefrontal cortex and hippocampus in mutation independent manner. We also found the increase in production by peritoneal macrophage cells on tumor necrosis factor alpha and interleukin 1beta after pro-inflammatory stimulation and increase in interleukin 4 productions in anti-inflammatory stimulation in both wt and mutant mice. CONCLUSIONS: The regulation of inflammatory process is a complex process in which a number of cells and molecules play different roles in a coordinated and well-controlled manner. Therefore, the lack of GR in noradrenergic cells might be too subtle and insufficient modification to cause disturbances in inflammatory responses after chronic stress. Supported by grant no. POIG.01.01.02-12-004/09 co-financed by the ERDF and by statutory funds of Institute of Pharmacology PAS.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2015
• Tom: 75
• Numer: Supl.
• Opis fizyczny: p.S81

Twórcy

autor

Kusmierczyk J.

• Department of Brain Biochemistry, Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland

autor

Chmielarz P.

• Department of Brain Biochemistry, Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland

autor

Trojan E.

• Department of Brain Biochemistry, Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland

autor

Roman A.

• Department of Brain Biochemistry, Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland

autor

Nalepa I.

• Department of Brain Biochemistry, Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland