PubMed · 5916327
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A Lungu, A Cristoveanu, M Bunea, A Tache. 1966. [Ecologic factors and adrenocortical function].. https://pubmed.ncbi.nlm.nih.gov/5916327/
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The expression of transcripts for type 1 interleukin-1 receptors (IL-1R1) were investigated utilizing reverse transcription-polymerase chain reaction (RT-PCR) techniques in male C57BL/6 mice. First, we measured IL-1R1 mRNA 1, 2, 6, and 12 h after a single injection of endotoxin lipopolysaccharide (LPS; 30 microg/mouse). IL-1R1 mRNA was measured in relevant tissues utilizing semiquantitative RT-PCR. IL-1R1 mRNA levels were significantly increased 2 and 6 h after one LPS injection group in comparison with the saline injection group in the hippocampus and testis. Next, we investigated the effect of repeated injections of LPS on IL-1R1 expression. LPS or saline were injected at 24-h intervals for 4 consecutive days. The mice were divided into four groups: (1) LPS injections for 4 days and LPS injection on day 5 (LPS-LPS); (2) LPS injections for 4 days and saline injection on day 5 (LPS-saline); (3) saline injections for 4 days and LPS injection on day 5 (saline-LPS); (4) saline injections for 4 days and saline injection on day 5 (saline-saline). The mice were sacrificed by decapitation 2 h after the last injection. In the hippocampus and pituitary gland, significant increases of IL-1R1 mRNA levels were observed in the saline-LPS group, however, the increases were attenuated in LPS-LPS group. IL-1R1 mRNA levels in the hypothalamus were unchanged in all four groups. In the adrenal gland and testis, IL-1R1 mRNA levels were significantly increased in the LPS-LPS group as well as saline-LPS group. These data demonstrate differential regulation of IL-1R1 mRNA by one and repeated endotoxin treatment and suggest the importance of the cytokines in mediating the effects of infectious challenge on brain, endocrine and immune function during endotoxemia.
Plasma levels of high density lipoprotein (HDL) cholesterol and its major protein component apolipoprotein (apo) A-I are significantly reduced in both acute and chronic inflammatory conditions, but the basis for this phenomenon is not well understood. We hypothesized that secretory phospholipase A(2) (sPLA(2)), an acute phase protein that has been found in association with HDL, promotes HDL catabolism. A series of HDL metabolic studies were performed in transgenic mice that specifically overexpress human sPLA(2) but have no evidence of local or systemic inflammation. We found that HDL isolated from these mice have a significantly lower phospholipid and cholesteryl ester and significantly greater triglyceride content. The fractional catabolic rate (FCR) of (125)I-HDL was significantly faster in sPLA(2) transgenic mice (4.08 +/- 0.01 pools/day) compared with control wild-type littermates (2.16 +/- 0.48 pools/day). (125)I-HDL isolated from sPLA(2) transgenic mice was catabolized significantly faster than (131)I-HDL isolated from wild-type mice after injection in wild-type mice (p < 0.001). Injection of (125)I-tyramine-cellobiose-HDL demonstrated significantly greater degradation of HDL apolipoproteins in the kidneys of sPLA(2) transgenic mice compared with control mice (p < 0.05). The fractional catabolic rate of [(3)H]cholesteryl ether HDL was significantly faster in sPLA(2)-overexpressing mice (6.48 +/- 0.24 pools/day) compared with controls (4.80 +/- 0.72 pools/day). Uptake of [(3)H] cholesteryl ether into the livers and adrenals of sPLA(2) transgenic mice was significantly enhanced compared with control mice. In summary, these data demonstrate that overexpression of sPLA(2) alone in the absence of inflammation causes profound alterations of HDL metabolism in vivo and are consistent with the hypothesis that sPLA(2) may promote HDL catabolism in acute and chronic inflammatory conditions.
Serotonin type 2A (5-HT(2A)) receptor-mediated neurotransmitter is known to activate hypothalamic-pituitary-adrenal (HPA) axis, regulate sleep-awake cycle, induce anorexia and hyperthermia. Interaction between melatonin and 5-HT(2A) receptors in the regulation of the sleep-awake cycle and head-twitch response in rat have been reported. Previous studies have shown that melatonin has suppressant effect on HPA axis activation, decreases core body temperature and induces hyperphagia in animals. However, melatonin interaction with 5-HT(2A) receptors in mediation of these actions is not yet reported. We have studied the acute effect of melatonin and its antagonist, luzindole on centrally administered (+/-)-1-(2, 5-dimethoxy-4-iodophenyl) 2-amino propane (DOI; a 5-HT(2A/2C) agonist)-induced activation of HPA axis, hypophagia and hyperthermia in 24-h food-deprived rats. Like ritanserin [(1 mg/kg, i.p.) 5-HT(2A/2C) antagonist], peripherally administered melatonin (1.5 and 3 mg/kg, i.p.) did not affect the food intake, rectal temperature or basal adrenal ascorbic acid level. However, pretreatment of rats with it significantly reversed DOI (10 microgram, intraventricular)-induced anorexia and activation of HPA axis. But the hyperthermia induced by DOI was not sensitive to reversal by melatonin. Mel(1) receptor subtype antagonist luzindole (5 microgram, intraventricular) did not modulate the DOI effect but antagonized the melatonin (3 mg/kg, i.p.) reversal of 5-HT(2A) agonist response. The present data suggest that melatonin reversal of DOI-induced hypophagia could be due to suppression of 5-HT(2A) mediated activation of HPA axis.