Effect of foot shock stress on the interferon-γ production of murine intestinal intraepithelial lymphocytes

Zhang, Xiumin; Okutsu, Mitsuharu; Kanemi, Osamu; Nagatomi, Ryoichi

doi:10.1016/j.imlet.2005.03.011

Cited by 12 publications

(7 citation statements)

References 33 publications

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“…In the present study, stress acted as an ideal physiological trigger instead of pharmacological triggers to induce plaque disruption. Previous studies have confirmed that both electric foot shock and noise stimulation are effective stressors for mice (8,13,23,24,27,35,44). Besides the hemodynamic effects, foot shock stress also affects inflammatory (8) and immunologic (24) function.…”

Section: Discussionmentioning

confidence: 93%

Atherosclerotic plaque disruption induced by stress and lipopolysaccharide in apolipoprotein E knockout mice

N¹,

Wang²,

Zhang³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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To establish an animal model with disruptions of atherosclerotic plaques, 96 male apolipoprotein E knockout (apoE(-/-)) mice were randomly divided into stress, lipopolysaccharide (LPS), stress+LPS, and control groups (n = 24 each). All mice were fed a high-fat diet throughout the experiment, and carotid atherosclerotic lesions were induced by placement of a constrictive perivascular collar. Four weeks after surgery, mice in the LPS and stress+LPS groups were intraperitoneally injected with LPS (1 mg/kg twice per week for 8 wk). Eight weeks after surgery, mice in the stress and stress+LPS groups were treated with intermittent physical stress (electric foot shock and noise stimulation) for 4 wk. Morphological analysis revealed a plaque disruption rate of 16.7% in control, 34.8% in LPS, 54.2% in stress, and 60.9% in stress+LPS groups. The disruption rates in stress and stress+LPS groups were both significantly higher than those of controls (P = 0.007 and P = 0.002, respectively). Luminal thrombosis secondary to plaque disruption was observed only in the stress+LPS group. Both stress and LPS stimulation significantly decreased fibrous cap thickness and increased macrophage and lipid contents in plaques. Moreover, the combination of stress and LPS stimulation further lowered cap thickness and enhanced accumulation of macrophages and expression of inflammatory cytokines and matrix metalloproteinases. Stress activated the sympathetic nervous system, as manifested by increased blood pressure and flow velocity. Plasma fibrinogen levels were remarkably elevated in the stress and stress+LPS groups. In conclusion, stress- and LPS-costimulated apoE(-/-) mice provide a useful model for studies of plaque vulnerability and interventions.

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Section: Discussionmentioning

confidence: 93%

Atherosclerotic plaque disruption induced by stress and lipopolysaccharide in apolipoprotein E knockout mice

N¹,

Wang²,

Zhang³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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“…Peters et al (22) suggested that nerve growth factor (NGF) may be involved in the stress‐induced neurogenic inflammatory response following sonic stress exposure. We have recently demonstrated that intermittent FS, which is also used as a psychoemotional stressor (23,24), prolongs the telogen stage and delays the induction of the subsequent anagen stage in the murine hair cycle after depilation (15). We have further suggested that increased levels of plasma corticosterone and/or increased generation of CRF in the skin under stress result in the prolongation of the telogen stage.…”

Section: Discussionmentioning

confidence: 99%

Foot shock stress prolongs the telogen stage of the spontaneous hair cycle in a non‐depilated mouse model

Katayama

Aoki

Suzuki

et al. 2007

Experimental Dermatology

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Background: There is an increasing evidence to indicate that stress can influence skin disease and cutaneous functions. Previous studies have shown that stress alters the murine hair cycle; however, these studies have been carried out by using mouse models in which the hair cycle is forcibly synchronized after depilation. Objective: To examine whether foot shock stress (FS) changes the spontaneous hair cycle in a non‐depilated animal model, and to evaluate the role of mast cells and substance P (SP) in the influence of stress on the hair cycle. Methods: Changes in the spontaneous hair cycle and the inhibitory effects of a specific SP NK1 receptor antagonist were examined in non‐depilated mice during 3–4 weeks of FS. Results: Foot shock stress prolonged the telogen stage of the hair cycle and delayed the induction of the subsequent anagen stage in the animal model. FS caused an increase in the ratio of de‐granulated mast cells in the skin, an increase in the number of TUNEL‐positive cells, and a decrease in the number of Ki67‐positive cells. The NK1 receptor antagonist, WIN 62577, inhibited these stress responses. Conclusion: Our results strongly support previous work, demonstrating that stress alters active hair‐cycling in vivo through the action of SP.

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“…The stress produced in rats by exposure to heat negatively affected some intestinal parameters, including the levels of CD3+ and CD4+ T lymphocytes, the expression of TLR-2 and TLR-4, as well as the transcriptional mRNA expression of IFN-γ and IL-2, -4, and -10 (Liu et al, 2012). Assays on rats with an electric shock protocol showed that stress suppressed the production of IFN-γ through T cells with TCRαβ in the intraepithelial compartment, while at the same time elevating the level of endogenous glucocorticoids (Zhang et al, 2005). Studies on rodents under psychological stress have also reported a decrease in levels of intestinal SIgA, caused by: (i) an expectation of electric foot shock (Yamamoto et al, 2009), (ii) a continuous back and forth transference from housing cages to metabolic cages (Eriksson et al, 2004), and (iii) immobilization, in some cases combined with exposure to loud noise (Ponferrada et al, 2007; Caso et al, 2009; Zoppi et al, 2012).…”

Section: The Restraint Model and The Influence Of Stress In The Intesmentioning

confidence: 99%

Stress modulates intestinal secretory immunoglobulin A

Campos-Rodrı́guez

Godínez‐Victoria

Abarca-Rojano

et al. 2013

Front. Integr. Neurosci.

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Stress is a response of the central nervous system to environmental stimuli perceived as a threat to homeostasis. The stress response triggers the generation of neurotransmitters and hormones from the hypothalamus pituitary adrenal axis, sympathetic axis and brain gut axis, and in this way modulates the intestinal immune system. The effects of psychological stress on intestinal immunity have been investigated mostly with the restraint/immobilization rodent model, resulting in an up or down modulation of SIgA levels depending on the intensity and time of exposure to stress. SIgA is a protein complex formed by dimeric (dIgA) or polymeric IgA (pIgA) and the secretory component (SC), a peptide derived from the polymeric immunoglobulin receptor (pIgR). The latter receptor is a transmembrane protein expressed on the basolateral side of gut epithelial cells, where it uptakes dIgA or pIgA released by plasma cells in the lamina propria. As a result, the IgA-pIgR complex is formed and transported by vesicles to the apical side of epithelial cells. pIgR is then cleaved to release SIgA into the luminal secretions of gut. Down modulation of SIgA associated with stress can have negative repercussions on intestinal function and integrity. This can take the form of increased adhesion of pathogenic agents to the intestinal epithelium and/or an altered balance of inflammation leading to greater intestinal permeability. Most studies on the molecular and biochemical mechanisms involved in the stress response have focused on systemic immunity. The present review analyzes the impact of stress (mostly by restraint/immobilization, but also with mention of other models) on the generation of SIgA, pIgR and other humoral and cellular components involved in the intestinal immune response. Insights into these mechanisms could lead to better therapies for protecting against pathogenic agents and avoiding epithelial tissue damage by modulating intestinal inflammation.

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Effect of foot shock stress on the interferon-γ production of murine intestinal intraepithelial lymphocytes

Cited by 12 publications

References 33 publications

Atherosclerotic plaque disruption induced by stress and lipopolysaccharide in apolipoprotein E knockout mice

Atherosclerotic plaque disruption induced by stress and lipopolysaccharide in apolipoprotein E knockout mice

Foot shock stress prolongs the telogen stage of the spontaneous hair cycle in a non‐depilated mouse model

Stress modulates intestinal secretory immunoglobulin A

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