Air pollution is associated with elevated HPA-Axis response to stress in anxious adolescent girls

Psoriasis is a chronic inflammatory skin disease with systemic manifestation, in which psychological factors play an important role. The etiology of psoriasis is complex and multifactorial, including genetic background and environmental factors such as emotional or physical stress. Psychological stress may also play a role in exacerbation of psoriasis, by dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis, sympathetic–adrenal–medullary axis, peripheral nervous system, and immune system. Skin cells also express various neuropeptides and hormones in response to stress, including the fully functional analog of the HPA axis. The deterioration of psoriatic lesions is accompanied by increased production of inflammatory mediators, which could contribute to the imbalance of neurotransmitters and the development of symptoms of depression and anxiety. Therefore, deregulation of the crosstalk between endocrine, paracrine, and autocrine stress signaling pathways contributes to clinical manifestations of psoriasis, which requires multidisciplinary approaches.

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Role of the basolateral amygdala in mediating the effects of the fatty acid amide hydrolase inhibitor URB597 on HPA axis response to stress

European Neuropsychopharmacology ◽

10.1016/j.euroneuro.2014.07.005 ◽

2014 ◽

Vol 24 (9) ◽

pp. 1511-1523 ◽

Cited By ~ 29

Author(s):

Gaurav Bedse ◽

Roberto Colangeli ◽

Angelo M. Lavecchia ◽

Adele Romano ◽

Fabio Altieri ◽

...

Keyword(s):

Fatty Acid ◽

Hpa Axis ◽

Basolateral Amygdala ◽

Fatty Acid Amide Hydrolase ◽

Acid Amide ◽

Response To Stress ◽

Amide Hydrolase ◽

Fatty Acid Amide

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The Defecation Index as a Measure of Emotionality: Questions Raised by HPA Axis and Prolactin Response to Stress in the Maudsley Model

Behavior Genetics ◽

10.1007/s10519-015-9722-x ◽

2015 ◽

Vol 45 (3) ◽

pp. 368-373 ◽

Cited By ~ 1

Author(s):

David A. Blizard ◽

J. Charles Eldridge ◽

Byron C. Jones

Keyword(s):

Hpa Axis ◽

Response To Stress ◽

Prolactin Response

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Antenatal Treatment with Glucocorticoids and the Hypotalamic-Pituitary-Adrenal Axis

Journal of Medical Biochemistry ◽

10.2478/jomb-2014-0038 ◽

2014 ◽

Vol 33 (4) ◽

pp. 307-316 ◽

Cited By ~ 1

Author(s):

Milica Manojlović-Stojanoski ◽

Nataša Ristić ◽

Sandra Singh ◽

Verica Milošević

Keyword(s):

Hpa Axis ◽

Fetal Development ◽

Adverse Outcomes ◽

Potent Effect ◽

Intrauterine Development ◽

Positive Effects ◽

Response To Stress ◽

Near Term ◽

Species Specific ◽

Synthetic Glucocorticoids

Summary Fetal development is a critical period in the life cycle which is why the placenta provides a structural and physiological barrier that protects the fetus from the outer fluctuations and inner disturbances. A variety of influences from the environment, however, might induce fetal overexposure to glucocorticoids that target the fetal hypothalamic-pituitary-adrenal (HPA) axis and influence the fetal growth trajecto-r y. Development of the HPA axis starts in the early stages of pregnancy, but the timing of HPA axis maturation and the glucocorticoid receptor (GR) expression in relation to birth is highly species-specific. The functional state of the fetal HPA axis plays a key role in the maturation of many organs necessary for intrauterine development and existence after birth. A functional HPA axis in near-term fetuses provides an adequate response to stress and also affects the timing of parturition. Due to their potent effect on the maturation of fetal tissues, synthetic glucocorticoids are used in human pregnancy at risk of preterm delivery. Dexamethasone and betamethasone, as the ones most commonly used, cross the placental enzymatic barrier (11b-hydroxysteroid dehydrogenase type 2 – 11b-HSD2) and have 25-fold higher affinity to the GR than endogenous glucocorticoids, stimulating many aspects of fetal maturation. Despite the numerous positive effects, exposure to synthetic glucocorticoids during fetal development may result in intrauterine growth retardation and fetal programming of the HPA axis function which is associated with cardiovascular, metabolic and psychiatric disorders manifested later in life. Long-term consequences indicate the need for the implementation of new studies that will provide a better understanding of the link between glucocorti-coid overexposure during fetal development and adverse outcomes in adulthood.

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Effect of glucocorticoid therapy on adrenal function in children with acute lymphoblastic leukemia

Paediatrica Indonesiana ◽

10.14238/pi54.1.2014.15-21 ◽

2014 ◽

Vol 54 (1) ◽

pp. 15

Author(s):

Gita Widyapuri ◽

Djajadiman Gatot ◽

Aman Bakti Pulungan ◽

Badriul Hegar

Keyword(s):

Hpa Axis ◽

Standard Dose ◽

Lymphoblastic Leukemia ◽

Adrenal Function ◽

High Dose ◽

Induction Phase ◽

Acth Test ◽

Before And After ◽

Response To Stress ◽

Cortisol Levels

BackgroundGlucocorticoids play an important role in thetreatment ofacute lymphoblastic leukemia (ALL), but can causeside effects such as suppression of the hypothalamic-pituitaryadrenal (HPA) axis. Suppression of the HPA axis causes adrenal insufficiency, disturbs the cortisol response to stress, and may be a cause of morbidity and mortality in children with ALL.ObjectiveTo evaluate adrenal function in children with ALL afterinduction chemotherapy with high dose glucocorticoids.MethodsThe adrenal function of 20 children with ALL wasevaluated using a standard dose (250 μ g) adrenocorticotropinhormone (ACTH) test performed before and after a 6 week oftreatment with glucocorticoids induction phase chemotherapy,which was followed by a week period tapering off. Adrenalinsuffien cy was defined as blood cortisol level of < 18 μg/dLResultsAdrenal insufficiency was found in 14/20 subjects afterthe induction phase followed by a week period of tapering off.Median cortisol levels pre- and post-stimulation before inductionphase were 14.72 (range 2.0 1- 46. 1) μg/dL and 29.29 (range 21.65 - 55 .15) μg/dL, respectively. Median cortisol levels pre- and poststimulation after induction phase were 5.87 (range 0.2 - 20.53)μg/dL and 10.49 (range 0.33 - 28.69) μg/dL, respectively. Clinicalsigns and symptoms did not differ between those with and withoutadrenal insufficiency.ConclusionOf 20 children with ALL, 14 develop adrenalinsufficiency after a 6-week induction therapy with glucocorticoidsand followed by a week period of tapering off. No specific clinicalsigns and symptoms are identified to be related to the adrenalinsufficiency.

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Minireview: Neuro-Immuno-Endocrine Modulation of the Hypothalamic-Pituitary-Adrenal (HPA) Axis by gp130 Signaling Molecules

Endocrinology ◽

10.1210/endo.143.5.8861 ◽

2002 ◽

Vol 143 (5) ◽

pp. 1571-1574 ◽

Cited By ~ 72

Author(s):

Vera Chesnokova ◽

Shlomo Melmed

Keyword(s):

Feedback Control ◽

Hpa Axis ◽

Prolonged Exposure ◽

Hormone Secretion ◽

Dominant Negative ◽

Cytokine Signaling ◽

Hypothalamic Pituitary Adrenal ◽

Pituitary Development ◽

Response To Stress ◽

Pomc Gene

Abstract The neuroendocrine and immune systems communicate bidirectionally. The neuro-immune-endocrine interface is mediated by cytokines acting as auto/paracrine or endocrine factors regulating pituitary development, cell proliferation, hormone secretion, and feedback control of the hypothalamic-pituitary-adrenal (HPA) axis. At birth or during neonatal ontogenesis, cytokines produce permanent alterations of HPA axis function and the stress response. Overexpressing IL-6 or leukemia inhibitory factor leads to significant changes in pituitary development and functions. Pituitary corticotroph POMC gene expression is regulated by CRH as well as several gp130 cytokines acting as neuro-immuno-endocrine modulators. Conversely, HPA axis functions modulate susceptibility or resistance to inflammatory disease. Cytokines (including IL-1, TNF, and members of the gp130 cytokine family) participate as mediators of a complex HPA axis response to stress and inflammation. Prolonged exposure to proinflammatory cytokines increases levels of the dominant negative glucocorticoid receptor isoform. Nonresponsiveness of the HPA axis to glucocorticoid negative feedback control provides a defense from destructive effects of cytokine excess. At the same time, gp130 cytokines stimulate pituitary suppressor of cytokine signaling (SOCS)-3, which represses cytokine signaling and abrogates cytokine-induced corticotroph POMC gene transcription and ACTH secretion.

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Interpersonal Stress Severity Longitudinally Predicts Adolescent Girls’ Depressive Symptoms: the Moderating Role of Subjective and HPA Axis Stress Responses

Journal of Abnormal Child Psychology ◽

10.1007/s10802-018-0483-x ◽

2018 ◽

Vol 47 (5) ◽

pp. 895-905 ◽

Cited By ~ 7

Author(s):

Sarah A. Owens ◽

Sarah W. Helms ◽

Karen D. Rudolph ◽

Paul D. Hastings ◽

Matthew K. Nock ◽

...

Keyword(s):

Depressive Symptoms ◽

Adolescent Girls ◽

Hpa Axis ◽

Stress Responses ◽

Interpersonal Stress ◽

Moderating Role

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Rats Lacking Dopamine Transporter Display Increased Vulnerability and Aberrant Autonomic Response to Acute Stress

Biomolecules ◽

10.3390/biom10060842 ◽

2020 ◽

Vol 10 (6) ◽

pp. 842

Author(s):

Placido Illiano ◽

Gregory E. Bigford ◽

Raul R. Gainetdinov ◽

Marta Pardo

Keyword(s):

Dopamine Transporter ◽

Hpa Axis ◽

Acute Stress ◽

Female Rats ◽

Autonomic Response ◽

Before And After ◽

Response To Stress ◽

Vulnerability To Stress ◽

Body Temperature Increase ◽

Reduced Temperature

The activity of the hypothalamus–pituitary–adrenal (HPA) axis is pivotal in homeostasis and presides the adaptative response to stress. Dopamine Transporter (DAT) plays a key role in the regulation of the HPA axis. We used young adult female DAT Knockout (KO) rats to assess the effects of DAT ablation (partial, heterozygous DAT+/-, or total, homozygous DAT-/-) on vulnerability to stress. DAT-/- rats show profound dysregulation of pituitary homeostasis, in the presence of elevated peripheral corticosterone, before and after acute restraint stress. During stress, DAT-/- rats show abnormal autonomic response at either respiratory and cardiovascular level, and delayed body temperature increase. DAT+/- rats display minor changes of hypophyseal homeostatic mechanisms. These rats display a similar pituitary activation to that of the control animals, albeit in the presence of higher release of peripheral corticosterone than DAT-/- after stress, and reduced temperature during stress. Our data indicate that DAT regulates the HPA axis at both the central and peripheral level, including autonomic function during stress. In particular, the partial deletion of DAT results in increased vulnerability to stress in female rats, which display central and peripheral alterations that are reminiscent of PTSD, and they might provide new insights in the pathophysiology of this disorder.

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