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Article

Lipopolysaccharide Challenge Reveals Hypothalamic-Pituitary-Adrenal Axis Dysfunction in Murine Systemic Lupus Erythematosus

Department of Physiology and Anatomy, University of North Texas Health Science Center, Fort Worth, TX 76107, USA
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Author to whom correspondence should be addressed.
Brain Sci. 2018, 8(10), 184; https://doi.org/10.3390/brainsci8100184
Received: 24 August 2018 / Revised: 28 September 2018 / Accepted: 2 October 2018 / Published: 4 October 2018
Crosstalk between the brain and innate immune system may be dysregulated in systemic lupus erythematosus (SLE), a chronic autoimmune disease that presents with dysautonomia and aberrant inflammation. The hypothalamic-pituitary-adrenal (HPA) axis is an endogenous neuro-endocrine-immune pathway that can regulate inflammation following activation of vagal afferents. We hypothesized that chronic inflammatory processes in SLE are in part due to HPA axis dysfunction, at the level of either the afferent vagal-paraventricular nuclei (PVN) interface, the anterior pituitary, and/or at the adrenal glands. To study this, we challenged female control and SLE mice with lipopolysaccharide (LPS) and measured c-Fos expression as an index of neuronal activation, plasma adrenocorticotrophic hormone (ACTH) as an index of anterior pituitary function, and plasma corticosterone as an index of adrenal function. We found that c-Fos expression in the PVN, and plasma ACTH and corticosterone were comparable between unchallenged SLE and control mice. PVN c-Fos was increased similarly in control and SLE mice three hours after LPS challenge; however, there were no changes in plasma ACTH amongst any experimental groups post inflammatory challenge. Plasma corticosterone was markedly increased in LPS-challenged SLE mice compared to their vehicle-treated counterparts, but not in controls. Paradoxically, following LPS challenge, brain and spleen TNF-α were elevated in LPS-challenged SLE mice despite heightened plasma corticosterone. This suggests that, despite normal c-Fos expression in the PVN and activation of the HPA axis following LPS challenge, this cumulative response may not adequately defend SLE mice against inflammatory stimuli, leading to abnormally heightened innate immune responses and peripheral inflammation. View Full-Text
Keywords: neuroimmune; vagus nerve; autoimmune disease; inflammation; corticosterone; cytokines neuroimmune; vagus nerve; autoimmune disease; inflammation; corticosterone; cytokines
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MDPI and ACS Style

Pham, G.S.; Mathis, K.W. Lipopolysaccharide Challenge Reveals Hypothalamic-Pituitary-Adrenal Axis Dysfunction in Murine Systemic Lupus Erythematosus. Brain Sci. 2018, 8, 184. https://doi.org/10.3390/brainsci8100184

AMA Style

Pham GS, Mathis KW. Lipopolysaccharide Challenge Reveals Hypothalamic-Pituitary-Adrenal Axis Dysfunction in Murine Systemic Lupus Erythematosus. Brain Sciences. 2018; 8(10):184. https://doi.org/10.3390/brainsci8100184

Chicago/Turabian Style

Pham, Grace S., and Keisa W. Mathis 2018. "Lipopolysaccharide Challenge Reveals Hypothalamic-Pituitary-Adrenal Axis Dysfunction in Murine Systemic Lupus Erythematosus" Brain Sciences 8, no. 10: 184. https://doi.org/10.3390/brainsci8100184

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