Maternal Deprivation and Early Weaning Modulate Experimental Allergic Encephalomyelitis in the Rat

Laban, Olgica; Marković, Biljana; Dimitrijević, Mirjana; Janković, Branislav D.

doi:10.1006/brbi.1995.1002

Cited by 44 publications

(18 citation statements)

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“…We found increased susceptibility to EAE after neonatal GC treatment. However, decreased susceptibility to autoimmunity in later life has been reported when rat pups were subjected to maternal deprivation from days 1-28 of life (28). Maternal deprivation is regarded as a stressor for the pups.…”

Section: Discussionmentioning

confidence: 99%

Neonatal Dexamethasone Treatment Increases Susceptibility to Experimental Autoimmune Disease in Adult Rats

Bakker

Kavelaars²,

Kamphuis

et al. 2000

The Journal of Immunology

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Major concern has emerged about the possible long term adverse effects of glucocorticoid treatment, which is frequently used for the prevention of chronic lung disease in preterm infants. Here we show that neonatal glucocorticoid treatment of rats increases the severity (p ≤ 0.01) and incidence (p ≤ 0.01) of the inflammatory autoimmune disease experimental autoimmune encephalomyelitis in adult life. In search of possible mechanisms responsible for the increased susceptibility to experimental autoimmune encephalomyelitis, we investigated the reactivity of the hypothalamo-pituitary-adrenal axis and of immune cells in adult rats after neonatal glucocorticoid treatment. We observed that neonatal glucocorticoid treatment reduces the corticosterone response after an LPS challenge in adult rats (p ≤ 0.001). Interestingly, LPS-stimulated macrophages of glucocorticoid-treated rats produce less TNF-α and IL-1β in adult life than control rats (p < 0.05). In addition, splenocytes obtained from adult rats express increased mRNA levels of the proinflammatory cytokines IFN-γ (p < 0.01) and TNF-β (p < 0.05) after neonatal glucocorticoid treatment. Apparently, neonatal glucocorticoid treatment has permanent programming effects on endocrine as well as immune functioning in adult life. In view of the frequent clinical application of glucocorticoids to preterm infants, our data demonstrate that neonatal glucocorticoid treatment may be a risk factor for the development of (auto)immune disease in man.

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Section: Discussionmentioning

confidence: 99%

Neonatal Dexamethasone Treatment Increases Susceptibility to Experimental Autoimmune Disease in Adult Rats

Bakker

Kavelaars²,

Kamphuis

et al. 2000

The Journal of Immunology

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“…13) and decreased plaque-forming cell responses. Laban et al (35) have noted that maternal deprivation exerts the opposite effects on susceptibility to EAE, where both the neurological and the histological signs of the inflammation are suppressed compared with those in control animals. However, these researchers also observed that early weaning of pups exacerbated both the clinical signs and the histological lesions of EAE.…”

Section: Postnatal Environment and Maternal Factorsmentioning

confidence: 99%

The maternal-neonatal neuro-immune interface: Are there long-term implications for inflammatory or stress-related disease?

Shanks

Lightman²

2001

J. Clin. Invest.

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Inflammatory stimuli reliably elicit hypothalamic-pituitary-adrenal (HPA) activation, and it is now established that the immune and HPA systems are mutually regulatory and that their interactions partly determine stress effects on immune function. What has not been extensively investigated, however, is the interactive nature of the development of the endocrine and immune systems and whether this might alter predisposition to inflammatory disease or stress-related pathologies. Increasing attention is now being focused on the role of early life environments determining longterm predisposition to disease, and a role for the HPA axis in disease predisposition is emerging.Stress generally refers to the condition where coping with actual or perceived stimuli alters the homeostatic state of the organism. The classic stress response involves the activation of central and peripheral catecholamine systems and HPA responses. Increased glucocorticoid levels are thought to protect the organism, both by providing energy substrates to deal with immediate environmental demands and by blocking potentially harmful overreaction by the immune system and other stress-reactive systems (1). However, to avoid immunosuppression and degenerative pathologies associated with increased glucocorticoid levels, the HPA stress response must terminate efficiently once the environmental demands are removed (2). Consequently, disturbances in endocrine-immune interactions upset the normal regulatory homeostatic balance and alter susceptibility to a variety of disease states associated with immune dysregulation (3).The physiological impact of stress is variable across individuals, and susceptibility to stress apparently depends on attributes of the organism, such as genetic endowment and age, and experiential factors, such as previous stress experiences, and early life events (4, 5). Indeed, the endocrine and immune systems and the CNS all respond to environmental pressures during development, and the interactive nature of these systems suggests that alterations in one system could have developmental consequences for the others and potential long-term implications for disease vulnerability. Plasticity in most developing physiological systems is thought to be of adaptive importance, enabling an organism to better meet the demands of the environment in which it matures and will most likely reside. However, the short-term reorganization or re-setting of regulatory systems to deal with immediate demands may also have long-term consequences for normal physiological function, thereby predisposing an organism to pathology. This may particularly be the case when the environmental pressures differ between development and adulthood.A number of epidemiological studies have indicated that nutritional factors early in life have long-term implications for cardiovascular and metabolic disease in adulthood. Most data suggest that maternal nutrition and limited intrauterine growth are responsible for reorganizing metabolic regulation and results in metabolic and car...

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“…The effects of certain environmental stimuli experienced during development can persist throughout the life of the animal especially if such stimuli have occurred during periods of maximal sensitivity, known as 'critical periods'. There are several examples of environmental regulation of neural development [1,2]. The effect of neonatal handling on behavioral and neuroendocrine responses to stress represents one of the classical models for the study of environmental regulation of neural development and function.…”

Section: Introductionmentioning

confidence: 99%

Postnatal Touch Stimulation Acutely Alters Corticosterone Levels and Glucocorticoid Receptor Gene Expression in the Neonatal Rat

et al. 2003

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Environmental manipulation early in life can alter the development of the hypothalamic-pituitary-adrenal (HPA) axis by mechanisms that are still unclear. The aim of the present work was to study the acute effects of postnatal touch stimulation, in an attempt to understand the mechanism by which touch stimulation early in life alters the HPA response to stress in adult animals. Rat pups were gently brushed for 15 min daily during the 1st postnatal week. Serum corticosterone levels were determined by radioimmunoassays, while glucocorticoid receptor (GR) gene expression was assayed by semiquantitative reverse transcriptase-polymerase chain reaction. Touch stimulation induced a significant decrease (30–36%) in serum corticosteroid secretion during the 1st and 2nd postnatal day as compared to the unstimulated group. In contrast, GR gene expression in the touch stimulation group was significantly increased in several brain areas such as the hippocampus (19–21%), frontal cortex (26–34%) and midbrain (15–24%). The results thus indicate that neonatal touch stimulation causes acute hormone- secretion and gene-expression changes within the period of stimulation. These changes may be the underlying cause for the permanent changes that have been observed in adult animals touch-stimulated as neonates.

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Maternal Deprivation and Early Weaning Modulate Experimental Allergic Encephalomyelitis in the Rat

Cited by 44 publications

References 0 publications

Neonatal Dexamethasone Treatment Increases Susceptibility to Experimental Autoimmune Disease in Adult Rats

Neonatal Dexamethasone Treatment Increases Susceptibility to Experimental Autoimmune Disease in Adult Rats

The maternal-neonatal neuro-immune interface: Are there long-term implications for inflammatory or stress-related disease?

Postnatal Touch Stimulation Acutely Alters Corticosterone Levels and Glucocorticoid Receptor Gene Expression in the Neonatal Rat

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