Regular ArticleAlterations in Hypothalamic–Pituitary–Adrenal Function Correlated with the Onset of Murine SLE in MRL +/+ and lpr/lpr Mice
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Neuropsychiatric systemic lupus erythematosus and cognitive dysfunction: The MRL-lpr mouse strain as a model
2014, Autoimmunity ReviewsCitation Excerpt :The stress-induced increase serum concentration of glucocorticoids is essential for the prevention of autoreactive or uncontrolled amplification of the immune response, which results in autoimmunity and self-injury. A defective HPA axis may then confer susceptibility to autoimmune disorders, and it seems that such a deficiency is present in both murine and human lupus [110,164,168]. Nowadays, studies on the function of the HPA axis are rather limited in patients with SLE and often confounded by the effect of concomitant glucocorticoid treatment.
Altered neuroendocrine status at the onset of CNS lupus-like disease
2013, Brain, Behavior, and ImmunityCitation Excerpt :Although far from being elucidated, the key point in understanding a dysfunctional HPA axis could lie in significant structural and functional changes in the PVN, the key interface structure between the nervous and endocrine systems. We and others have previously reported upregulated arginine-vasopressin signal expression, as well as enhanced Ki67, Fluoro Jade B and H&E staining in the PVN of diseased MRL/lpr mice (Sakic et al., 1999; Shanks et al., 1999; Ballok et al., 2003a,b; Stanojcic et al., 2009, 2010). More recently, a similar discrepancy in PVN H&E staining was observed when 17-week old 485 mice were compared to age-matched 6825 mice (Loheswaran et al., 2010).
Intrathecal antibodies and brain damage in autoimmune MRL mice
2010, Brain, Behavior, and ImmunityDisturbed distribution of proliferative brain cells during lupus-like disease
2009, Brain, Behavior, and ImmunityCitation Excerpt :Similarly, a group of PVN parvocellular neurons co-secrete AVP and CRH into the anterior pituitary by projecting through the ME (Kupfermann, 1991). Consistent with the above, imbalanced AVP/CRH mRNA expression ratio in the PVN (Sakic et al., 1999; Shanks et al., 1999) and disturbed activity of the hypothalamus–pituitary-adrenal axis are reported in MRL/lpr mice (Hu et al., 1993; Lechner et al., 1996; Lechner et al., 2000). The role of Ki67+/BrdU− neurons in the PVN and AVP overexpression may be of particular importance in understanding the etiology of endocrine and behavioral deficits in the MRL model and SLE patients.
Purine receptor antagonist modulates serology and affective behaviors in lupus-prone mice: Evidence of autoimmune-induced pain?
2008, Brain, Behavior, and ImmunityCitation Excerpt :When considering that suramin does not significantly cross the BBB or the blood–CSF barrier (Sanderson et al., 2007), and that neuronal atrophy did not arise in drug treated MRL +/+ animals, it was unlikely that dendritic aberrations in the hippocampus of MRL-lpr animals were a by-product of treatment. Since chronic administration of corticosterone in drinking water, however, severely deteriorated neuronal morphology of asymptomatic animals, CA1 atrophy may be induced by an autoimmunity-sustained upregulation of corticosterone production in MRL-lpr animals (Shanks et al., 1999). Given that a low-calorie diet completely prevents splenomegaly and autoimmunity in MRL-lpr animals (Fernandes and Good, 1984), inborn errors in metabolism appear to underlie the dysregulation of neuro-immuno-endocrine networks that manifest disease.
Chapter 9 Adrenal Involvement in Systemic Autoimmune Diseases
2008, Handbook of Systemic Autoimmune DiseasesCitation Excerpt :A significantly lower increase in plasma corticosteroid concentrations after stimulation with recombinant IL-1 has been demonstrated in the MRL/lpr murine model of lupus (Lechner et al., 2000). In addition, aging of mice, which is accompanied by increased autoantibody production, is associated with a decrease in hypothalamic expression of the CRH-mRNA (Shanks et al., 1999). Studies of the HPA axis in patients with SLE are limited and often influenced by concomitant glucocorticoid treatment.