HPA-axis responses during experimental colitis in the rat

Kojima, Kensaku; Naruse, Yoshihisa; Iijima, Norio; Wakabayashi, Naoki; Mitsufuji, Shoji; Ibata, Yasuhiko; Tanaka, Masaki

doi:10.1152/ajpregu.00260.2001

Cited by 20 publications

(23 citation statements)

References 46 publications

(50 reference statements)

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“…The condition under which we have previously demonstrated enhanced weight loss in our P14 LPS-treated rats, experimental colitis, can be regarded as extremely stressful (28,53) and is representative only of individuals suffering from inflammatory bowel disease, a condition in which weight loss is evident regardless of neonatal experience (56). In the present study, we examined body weight under physiological conditions more likely to be experienced by the general population.…”

mentioning

confidence: 93%

Neonatal immune challenge does not affect body weight regulation in rats

Spencer¹,

Mouihate²,

Galic³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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The perinatal environment plays a crucial role in programming many aspects of adult physiology. Myriad stressors during pregnancy, from maternal immune challenge to nutritional deficiency, can alter longterm body weight set points of the offspring. In light of the increasing concern over body weight issues, such as obesity and anorexia, in modern societies and accumulating evidence that developmental stressors have long-lasting effects on other aspects of physiology (e.g., fever, pain), we explored the role of immune system activation during neonatal development and its impact on body weight regulation in adulthood. Here we present a thorough evaluation of the effects of immune system activation (LPS, 100 g/kg ip) at postnatal days 3, 7, or 14 on long-term body weight, adiposity, and body weight regulation after a further LPS injection (50 g/kg ip) or fasting and basal and LPS-induced circulating levels of the appetite-regulating proinflammatory cytokine leptin. We show that neonatal exposure to LPS at various times during the neonatal period has no long-term effects on growth, body weight, or adiposity. We also observed no effects on body weight regulation in response to a short fasting period or a further exposure to LPS. Despite reductions in circulating leptin levels in response to LPS during the neonatal period, no long-term effects on leptin were seen. These results convincingly demonstrate that adult body weight and weight regulation are, unlike many other aspects of adult physiology, resistant to programming by a febrile-dose neonatal immune challenge.gender; leptin; lipopolysaccharide; obesity THE PERINATAL ENVIRONMENT is known to play a crucial role in programming body weight. In humans, low birth weight and malnutrition during gestation have been linked with abdominal obesity in adulthood (31,45,46). Similarly, a variety of behavioral, physiological (including dietary manipulations), and immune stressors given to pregnant experimental animals have been reported to alter the body weight of adult offspring (4,15,27,36,40,63). It appears, however, that the timing of perinatal stress is critical in programming many aspects of adult physiology (35) and relatively little is known regarding the influence of postnatal stress on adult body weight regulation.The long-term physiological consequences of a neonatal immune challenge with LPS have been extensively described by our laboratory and others. For example, we have shown attenuated febrile and associated host defense responses in adulthood to an immune challenge of the same type as that experienced at postnatal day (P) 14 (9,17,18). Changes have also been demonstrated in memory processing (7), hypothalamic-pituitary-adrenal axis activation (51, 52), and susceptibility to pathological insults in adulthood (10, 55, 56). However, the long-term effects of a neonatal immune challenge on body weight regulation are less clear, and given the concern over the current obesity epidemic in modern society [e.g., (29)], demand further investigation. For instance, Walker ...

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mentioning

confidence: 93%

Neonatal immune challenge does not affect body weight regulation in rats

Spencer¹,

Mouihate²,

Galic³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…It has become evident in recent years that the immune system is closely involved with stress-relieving mechanisms, in particular in relation to the nervous and endocrine systems. 4 In a study in rats, Kojima et al 5 showed that persistent infl ammatory stress from chronic colitis causes increased production of glucocorticoids, the fi nal product of the HPA-axis, and that these applied persistent negative feedback to the hypothalamus and pituitary glands. In a rat colitis model, Kresse et al 6 found that the HPAaxis is chronically activated, suggesting that overexpression of stress hormones upsets its functional balance.…”

Section: Introductionmentioning

confidence: 99%

Stress maladjustment in the pathoetiology of ulcerative colitis

et al. 2007

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“…This indicates that in physiological conditions the central CRH is regulated by the inhibitory feedback of cortisol that acts as a controlling factor of the inflammation. In rats, adrenalectomy and cortisol pellet replacement result in a marked increase in CRH mRNA, confirming the inhibitory feedback exerted by glucocorticoids in reaction to stress [62] . This study is supported by the results from Million et al [50] suggesting the protective role of CRH in stress-induced worsening of colitis.…”

Section: Hpa Responsementioning

confidence: 62%

Role of the Brain-Gut Axis in the Pathophysiology of Crohn’s Disease

Stasi

Orlandelli

2008

Dig Dis

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Studies on the interaction between the central nervous system and the gastrointestinal system have shed light on the neurobiological response to stress via the hypothalamic-pituitary-adrenal and the hypothalamic-autonomic nervous system axes. These findings support a role of psychological and environmental factors in the course of gastrointestinal disorders and their influence on the neuroendocrine regulation of the immune system. Crohn’s disease (CD) is a chronic inflammatory condition of the gastrointestinal tract, whose etiology involves genetic, psychological, immune and inflammatory factors. A higher prevalence of psychiatric diagnosis has been observed in CD patients. Both longitudinal and cross-sectional studies have explored the relationship between psychological stress and severity and/or clinical course of CD, with different, even conflicting, results. In several chronic diseases and stress-related psychological disorders, an alteration has been observed of the HPA response that through glucocorticoids modulate the immune/inflammatory reaction. In animal models of colitis, psychological or environmental stress may increase gastrointestinal permeability, allowing abnormal antigen presentation to the immune system and leading to the exacerbation and perpetuation of intestinal inflammation. The increased intestinal permeability under stress is mediated by corticotropin-releasing hormone stimulation through nicotinic, adrenergic and cholinergic receptors, suggesting a complex interplay between sympathetic and parasympathetic nervous systems. This review will examine and discuss the relationship between psychological stress and CD, investigating the role played by the hypothalamic-pituitary-adrenal and the hypothalamic-autonomic nervous system axes in stress-related psychological disorders, and the possible influence of chronic stress on the intestinal inflammation, in particular in CD.

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HPA-axis responses during experimental colitis in the rat

Cited by 20 publications

References 46 publications

Neonatal immune challenge does not affect body weight regulation in rats

Neonatal immune challenge does not affect body weight regulation in rats

Stress maladjustment in the pathoetiology of ulcerative colitis

Role of the Brain-Gut Axis in the Pathophysiology of Crohn’s Disease

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