Cytokines and neuro–immune–endocrine interactions: a role for the hypothalamic–pituitary–adrenal revolving axis

Haddad, John J.; Saadé, Nayef E.; Safieh‐Garabedian, Bared

doi:10.1016/s0165-5728(02)00357-0

Cited by 377 publications

(245 citation statements)

References 121 publications

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“…an immune response) (Elsasser et al, 1997(Elsasser et al, , 2008. Furthermore, intake and appetite are suppressed during stressful events (Haddad et al, 2002) with intake of nutrients by stressed livestock often compromised and below that normally consumed by unstressed animals (Duff and Galyean, 2007). Weaning under modern cattle production systems may be described as a multi-factorial stressor as it incorporates nutritional, physical and psychological elements (Weary et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Biomarker responses to weaning stress in beef calves

O'Loughlin

McGee

Doyle

et al. 2014

Research in Veterinary Science

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A B S T R A C TThe study objective was to investigate the physiological effects of weaning on beef calves and identify a panel of blood-based welfare biomarkers. On the day (d) of weaning (d 0), 16 spring-born, singlesuckled, beef bull calves that previously grazed with their dams at pasture, were assigned to one of two treatments: (1) control (n = 8), calves were loose-housed with their dam, (2) weaned (n = 8), calves were abruptly separated from their dam and loose-housed. Jugular blood was collected on d −4, 0, 1, 2, 3, 7, and 14 relative to weaning (d 0) and assayed for inflammatory and steroid variables. Total leukocyte counts were measured in whole blood. It is concluded that neutrophil number is a robust biomarker of stress and that plasma CXCL8 is a sensitive indicator of stress in weaned and control calves. In future studies, these two biomarkers should be central to the characterisation of stress responses.

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Section: Discussionmentioning

confidence: 99%

Biomarker responses to weaning stress in beef calves

O'Loughlin

McGee

Doyle

et al. 2014

Research in Veterinary Science

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“…This possibility is certainly plausible, because leptin is merely one of the many factors that regulate the hypothalamus and the pituitary and adrenal glands. These tissues produce multiple immunomodulatory hormones and neurotransmitters, 34 and recent evidence suggests that such neurohumoral factors directly mediate many aspects of the ob/ob (leptindeficient) phenotype. For example, leptin deficiency decreases NE, 14 and reduced NE is predominately responsible for the hypotension, hyperostosis, and peripheral adiposity that develops in ob/ob mice.…”

Section: Discussionmentioning

confidence: 99%

Norepinephrine regulates hepatic innate immune system in leptin-deficient mice with nonalcoholic steatohepatitis

Oben

Yang

et al. 2004

Hepatology

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It is not known why natural killer T (NKT) cells, which modulate liver injury by regulating local cytokine production, are reduced in leptin-deficient ob/ob mice. NKT cells express adrenoceptors. Thus, we hypothesize that the low norepinephrine (NE) activity of ob/ob mice promotes depletion of liver NKT cells, thereby sensitizing ob/ob livers to lipopolysaccharide (LPS) toxicity. To evaluate this hypothesis, hepatic NKT cells were quantified in wild-type mice before and after treatment with NE inhibitors, and in dopamine ␤-hydroxylase knockout mice (which cannot synthesize NE) and ob/ob mice before and after 4 weeks of NE supplementation. Decreasing NE activity consistently reduces liver NKT cells, while increasing NE has the opposite effect. Analysis of hepatic and thymic NKT cells in mice of different ages demonstrate an age-related accumulation of hepatic NKT cells in normal mice, while liver NKT cells become depleted after birth in ob/ob mice, which have increased apoptosis of hepatic NKT cells. NE treatment inhibits apoptosis and restores hepatic NKT cells. In ob/ob mice with reduced hepatic NKT cells, hepatic T and NKT cells produce excessive T helper (Th)-1 proinflammatory cytokines and the liver is sensitized to LPS toxicity. NE treatment decreases Th-1 cytokines, increases production of Th-2 cytokines, and reduces hepatotoxicity. Studies of CD1d-deficient mice, which lack the receptor required for NKT cell development, demonstrate that they are also unusually sensitive to LPS hepatotoxicity. In conclusion, low NE activity increases hepatic NKT cell apoptosis and depletes liver NKT cells, promoting proinflammatory polarization of hepatic cytokine production that sensitizes the liver to LPS toxicity. (HEPATOLOGY 2004;40:434 -441.)

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“…Cytokine IL-2 exerts numerous effects within the immune as well as the central nervous system and is thought to serve as a humoral signal in their communication at different levels of regulation (194). The data indicate that IL-2 and IL-6 are potent activators of the HPA axis, which provide additional evidence to support the hypothesis that hypercortisolemia in schizophrenia may be mediated by the elevated cytokines (195).…”

Section: The Immunological Markersmentioning

confidence: 78%