Sound Stress Research Articles

Stress Testing in the Aftermath of the Financial Crisis

Recent turmoil in the capital markets has showed again the vulnerability of the international financial system and highlighted the need for efficient stress testing of financial institutions trading and lending books. In fact, the severity of current European sovereign bonds crisis is primarily attributable to its unexpected nature and a more rigorous application of stress testing could have probably contributed to reduce the repercussions of this crisis. Under these circumstances, stress testing has become a primary concern for international policy makers and regulators who are continuously working on solution to address the vulnerabilities identified. In such a context, the Basel Committee on Banking Supervision is also attempting to reinforce principles for sound stress testing in risk governance practices, and an important part of the Supervisory Review Process and the Pillar 2 requirements are related to this subject matter.

스트레스 음파 처리에 따른 아메리카잎굴파리(Liriomyza trifolii)의 생리 변화와 프로테오믹 분석

본 연구는 음파 처리에 따른 아메리카잎굴파리(Liriomyza trifolii)의 생리 변화를 발육 시기별로 분석하였다. 유충의 섭식량은 섭식을 통해 형성된 잎 내부 갱도의 길이로 분석했다. 이때 5,000 Hz (95 dB)의 음파 처리는 섭식 행동을 크게 둔화시켰다. 이러한 스트레스 음파는 또한 용발육에 영향을 주어 315 - 5,000 Hz 음파 범위에서 발육 지연 효과를 나타냈고, 1,000 - 5,000 Hz 음파 범위에서 우화를 억제하였다. 스트레스 음파는 암컷의 산란 행동을 억제시켰으나 성충의 주광성 행동에는 영향을 주지 않았다. 스트레스 음파(5,000 Hz, 95 dB)를 받은 용은 이차원 전기영동 분석 결과 단백질 발현 양상에서 무처리구와 뚜렷한 차이를 보였다. 특정 단백질에 대한 MALDI-TOF 분석 결과는 trafficking protein particle complex I, triosephosphate isomerase, hypothetical protein TcasGA2_TC013388, polycystin-2, paraneoplastic neuronal antigen MA1 및 tropomyosin I (isoform M)의 단백질들이 무처리구에서 발견되고, 음파 처리구에서는 소멸되었다. 반면에 DOCK9, cytoskeletal keratin II 및 <TEX>$F_0F_1$</TEX>-ATP synthase beta subunit은 스트레스 음파 처리에 따라 새롭게 나타나는 단백질로 판명되었다. 이러한 스트레스 음파는 아메리카잎굴파리의 살충제에 대한 감수성을 크게 증가시켰다. 이상의 결과는 아메리카잎굴파리의 생리 과정을 교란하는 스트레스 음파가 작용한다는 것을 제시하고 있다. 또한 본 연구는 이러한 스트레스 음파를 이용하여 아메리카잎굴파리에 대한 새로운 물리적 해충 방제 기술 개발 가능성을 제시하고 있다. This study investigated the adverse effects of sound treatment on physiological processes of the American leafminer, Liriomyza trifolii, during several developmental stages. Larval feeding activity was analyzed by measuring feeding tunnel length. It was significantly suppressed by sound treatment (5,000 Hz, 95 dB). Sound treatment delayed the pupal period at 315 - 5,000 Hz and prevented adult emergence at 1,000 - 5,000 Hz. Female oviposition was also inhibited by the stress sound treatments. However, phototactic adult movement was not affected by sound treatment. Pupae treated with 5,000 Hz showed marked changes in protein patterns analyzed by two dimensional electrophoresis. MALDI-TOF analysis of specific protein spots indicated that trafficking protein particle complex I, triosephosphate isomerase, hypothetical protein TcasGA2_TC013388, polycystin-2, paraneoplastic neuronal antigen MA1, and tropomyosin I (isoform M) were predicted in the control insects and disappeared in the insects treated with sound. By contrast, DOCK9, cytoskeletal keratin II, and F0F1-ATP synthase beta subunit were predicted only in the sound-treated insects. Furthermore, stress sound significantly increased the susceptibility of L. trifolii to insecticides. These results suggest that physiological processes of L. trifolii are altered by sound stress, which may be exploited to develop a novel physical control tactic against L. trifolii.

Stress increases VCAM-1 expression at the fetomaternal interface in an abortion-prone mouse model

Sound stress exposure increases fetal loss via inflammatory pathways. Inflammation is known to up-regulate cell adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1), which mediates the adhesion of leukocytes to the vascular endothelium. In this work, we studied the frequency of VCAM-1(+) vessels at the fetomaternal interface in stressed and non-stressed pregnant CBA/J female mice mated with DBA/2J (high fetal loss model) or BALB/c (low fetal loss model) males. The high fetal loss model had fewer large vessels on gestation day 6.5, and stress reduced the frequency of large vessels to a similar number in both high and low fetal loss models. In the high fetal loss model, however, the frequency of VCAM-1+ vessels was dramatically increased. This study shows that VCAM-1 expression is modulated by stress at the fetomaternal interface in abortion-prone cross-breeding.

A design model for strain-softening and strain-hardening fiber reinforced elements reinforced longitudinally with steel and FRP bars

A close-form solution is developed for the prediction of the moment–curvature relationship of cross sections of fiber reinforced concrete (FRC) elements failing in bending, and reinforced longitudinally with steel and fiber reinforced polymer (FRP) bars. The FRP bars are installed with the largest possible internal arm, e.g. with the minimum concrete cover that assures the bond conditions for a sound stress transfer from FRC to the FRP bars. The model is also able of simulating the flexural strengthening contribution provided by FRP bars installed according to the near surface mounted (NSM) technique. To have good protection conditions against corrosion, the steel bars are applied with a relatively thick FRC cover. Since steel stirrups are the reinforcement with the smaller concrete cover thickness, they are the most susceptible to corrosion. In the reinforcement concept to be developed in the present research program, steel stirrups are replaced with discrete fibers. This hybrid reinforcement aims to develop high durable pre-fabricated elements that fail in bending. The proposed analytical formulation can simulate FRC with strain softening or strain hardening behavior. In the present work, the formulation is described and its predictive performance is appraised.

Further Validation of a Model of Fibromyalgia Syndrome in the Rat

We have recently developed an animal model of fibromyalgia syndrome in the rat. In this model, rats exposed to unpredictable sound stress develop a delayed onset enhancement and prolongation of cytokine-induced mechanical hyperalgesia in muscle and skin. In this study, we tested the hypothesis that our model also manifests symptoms of common comorbid diagnoses: irritable bowel syndrome, temporomandibular disorder, and anxiety. Both visceral sensitivity and cytokine hyperalgesia in masseter muscle were present in the stressed rats. Furthermore, in an established model of irritable bowel syndrome—water avoidance—we observed significant muscle hyperalgesia. Finally, using the elevated plus maze to assess for anxiety level, we observed a significantly higher anxiety level in sound stress-exposed rats. Thus, unpredictable sound stress produces a condition in the rat with several features—delayed onset visceral and temporomandibular hyperalgesia and increased anxiety, as well as cutaneous and muscle hyperalgesia—commonly found in patients with fibromyalgia syndrome. Perspective A stress model—unpredictable sound—in the rat exhibits several features (cutaneous, musculoskeletal, and visceral hyperalgesia, as well as anxiety) that are found in patients with fibromyalgia syndrome. Thus, this model may be used to test hypotheses about the underlying mechanisms and response to therapy in patients with fibromyalgia.

Enhanced cytokine-induced mechanical hyperalgesia in skeletal muscle produced by a novel mechanism in rats exposed to unpredictable sound stress

Stress exacerbates both experimental and clinical pain, most well-characterized in irritable bowel and fibromyalgia syndromes. Since it has been hypothesized that cytokines play an etiopathogenic role in fibromyalgia and other chronic widespread pain conditions, we investigated the relationship between stress and cytokines in a model of stress-induced chronic somatic pain. A series of experiments were performed to evaluate the impact of stress on the hyperalgesia-induced by endotoxin (lipopolysaccharide, LPS) and the role of two pro-inflammatory cytokines, interleukin-6 (IL-6) and tumor necrosis α (TNFα). Fourteen days after exposure to a 4-day protocol of unpredictable sound stress, the ability of systemic LPS (100 μg/kg, i.p) to elicit cytokine-mediated mechanical hyperalgesia was measured in gastrocnemius muscle. LPS-induced hyperalgesia was significantly greater in stressed rats, but when rats were treated intrathecally with antisense oligodeoxynucleotide (ODN), to decrease either the gp130 subunit of the IL-6 receptor or the TNFα receptor, in nociceptors, skeletal muscle hyperalgesia in sound stressed, but not control, rats was prevented. These data suggest that chronic stress alters signaling in the primary afferent nociceptor for the hyperalgesia induced by endogenously produced pro-inflammatory cytokines.

The influence of long term sound stress on histological structure of broiler’s adrenal glands

The aim of this paper is to examine the effect of different sound stress duration on adrenal gland of broiler chickens of different age. The experiments were conducted on 90 HYBRO broiler chickens, divided into nine groups (each group consisting of 10 birds) by different age and lenght of sound stress duration. The chickens were exposed to sound stress in sound attenuated building using a fire alarm bell (95 dB) for stress sessions lasted 120 min every day. The histological structure of adrenal gland was analyzed by light microscopy. The results indicate that adrenal gland is sensitive on this kind of stress and sound as stressor could introduce organism in stress reaction. Adrenal glands of broilers exposed to sound stress characterized by marked hyperemia, hypertrophy of interrenal cells, smaller affinity for staining of chromaffin cells compared with control groups. According to our results, degree of histological changes of adrenal gland under the influence of sound stress depends on the length of exposure and age of chickens.

OS14F029 A Conventional Growth Estimation Formula of the Representative Surface Crack Replacing Plural Surface Cracks Generated at the Sound Stress Concentration Site

OS14F029 A Conventional Growth Estimation Formula of the Representative Surface Crack Replacing Plural Surface Cracks Generated at the Sound Stress Concentration Site

OS14-3-1 A Conventional Growth Estimation Formula of the Representative Surface Crack Replacing Plural Surface Cracks Generated at the Sound Stress Concentration Site

OS14-3-1 A Conventional Growth Estimation Formula of the Representative Surface Crack Replacing Plural Surface Cracks Generated at the Sound Stress Concentration Site

The WAG/Rij strain: A genetic animal model of absence epilepsy with comorbidity of depressiony

A great number of clinical observations show a relationship between epilepsy and depression. Idiopathic generalized epilepsy, including absence epilepsy, has a genetic basis. The review provides evidence that WAG/Rij rats can be regarded as a valid genetic animal model of absence epilepsy with comorbidity of depression. WAG/Rij rats, originally developed as an animal model of human absence epilepsy, share many EEG and behavioral characteristics resembling absence epilepsy in humans, including the similarity of action of various antiepileptic drugs. Behavioral studies indicate that WAG/Rij rats exhibit depression-like symptoms: decreased investigative activity in the open field test, increased immobility in the forced swimming test, and decreased sucrose consumption and preference (anhedonia). In addition, WAG/Rij rats adopt passive strategies in stressful situations, express some cognitive disturbances (reduced long-term memory), helplessness, and submissiveness, inability to make choice and overcome obstacles, which are typical for depressed patients. Elevated anxiety is not a characteristic (specific) feature of WAG/Rij rats; it is a characteristic for only a sub-strain of WAG/Rij rats susceptible to audiogenic seizures. Interestingly, WAG/Rij rats display a hyper-response to amphetamine similar to anhedonic depressed patients. WAG/Rij rats are sensitive only to chronic, but not acute, antidepressant treatments, suggesting that WAG/Rij rats fulfill a criterion of predictive validity for a putative animal model of depression. However, more and different antidepressant drugs still await evaluation. Depression-like behavioral symptoms in WAG/Rij rats are evident at baseline conditions, not exclusively after stress. Experiments with foot-shock stress do not point towards higher stress sensitivity at both behavioral and hormonal levels. However, freezing behavior (coping deficits) and blunted response of 5HT in the frontal cortex to uncontrollable sound stress, increased c-fos expression in the terminal regions of the meso-cortico-limbic brain systems and greater DA response of the mesolimbic system to forced swim stress suggest that WAG/Rij rats are vulnerable to some, but not to all types of stressors. We propose that genetic absence epileptic WAG/Rij rats have behavioral depression-like symptoms, are vulnerable to stress and might represent a model of chronic low-grade depression (dysthymia). Both 5HT and DAergic abnormalities detected in the brain of WAG/Rij rats are involved in modulation of vulnerability to stress and provocation of behavioral depression-like symptoms. The same neurotransmitter systems modulate SWDs as well. Recent studies suggest that the occurrence and repetition of absence seizures are a precipitant of depression-like behavior. Whether the neurochemical changes are primary to depression-like behavioral alterations remains to be determined. In conclusion, the WAG/Rij rats can be considered as a genetic animal model for absence epilepsy with comorbidity of dysthymia. This model can be used to investigate etiology, pathogenic mechanisms and treatment of a psychiatric comorbidity, such as depression in absence epilepsy, to reveal putative genes contributing to comorbid depressive disorder, and to screen novel psychotropic drugs with a selective and/or complex (dual) action on both pathologies.

Fetal origin of allergic asthma: insights on mechanistic cues and therapeutic targets arising from a mouse model of prenatal stress challenge

Background Prenatal stress challenge is a pivotal environmental factor which has been proposed to increase the vulnerability of offspring to develop chronic immune diseases in later life. We analyze the effect of prenatal exposure to stress during late gestation in mice. Materials and methods BALB/c mice were exposed to sound stress during late gestation. Maternal serum and placentas were analyzed. Fetal development was scored. Allergic asthma was induced in the offspring by using an ovalbumin protocol. We analyzed immune cells in lungs, bronchioalveolar fluid (BAL) and lung-draining lymph nodes as well as cytokine concentrations in the BAL. Further, stress-challenged pregnant females were treated with a progesterone derivative, followed by fetal analyses and evaluation of the vulnerability towards asthma in the offspring. Results Stress challenge resulted in decreased serum levels of maternal progesterone and testosterone, and increased serum levels of estradiol associated with placental endocrine dysfunction, such as low expression of proliferin. Fetal development was impaired upon stress challenge, especially in females. Prenatally stressed female adult offspring revealed an increased susceptibility toward asthma, mirrored by an increased airway response, influx of inflammatory cells and increased T helper 2 cytokines in the BAL. Further, we observed decreased frequencies of regulatory T cells (CD3 + CD4 + CD25 + foxP3 +) . Progesterone supplementation abrogated the impaired intrauterine development as well as the susceptibility toward asthma. Conclusions Our study revealed that prenatal stress severely interferes with the intrauterine development, resulting in offspring with an increased vulnerability toward asthma-like symptoms. Supplementation of progesterone during stress-challenged pregnancies abrogates gender-dependently the increased susceptibility toward asthma.

Attenuation of Activity in an Endogenous Analgesia Circuit by Ongoing Pain in the Rat

Analgesic efficacy varies depending on the pain syndrome being treated. One reason for this may be a differential effect of individual pain syndromes on the function of the endogenous pain control circuits at which these drugs act to produce analgesia. To test this hypothesis, we examined the effects of diverse (i.e., ongoing inflammatory, neuropathic, or chronic widespread) pain syndromes on analgesia induced by activation of an opioid-mediated, noxious stimulus-induced endogenous pain control circuit. This circuit was activated by subdermal capsaicin injection at a site remote from the site of nociceptive testing. Analgesia was not affected by carrageenan-induced inflammatory pain or the early phase of oxaliplatin neuropathy (a complication of cancer chemotherapy). However, the duration of analgesia was markedly shorter in the late phase of oxaliplatin neuropathy and in alcoholic neuropathy. A model of fibromyalgia syndrome produced by chronic unpredictable stress and proinflammatory cytokines also shortened analgesia duration, but so did the same stress alone. Therefore, since chronic pain can activate neuroendocrine stress axes, we tested whether they are involved in the attenuation of analgesic duration induced by these pain syndromes. Rats in which the sympathoadrenal axis was ablated by adrenal medullectomy showed normal duration pain-induced analgesia in groups with either late-phase oxaliplatin neuropathy, alcoholic neuropathy, or exposure to sound stress. These results support the suggestion that pain syndromes can modulate activity in endogenous pain control circuits and that this effect is sympathoadrenal dependent.

The influence of long term sound stress on histological structure of immune organs in broiler chickens

The aim of this paper was to examine the effect of different duration sound stress on immune organs of broiler chickens of different age. Nine groups, with 10 chickens in each group were included in experiment. The histological structure of bursa of Fabricius, thymus, and spleen were analyzed. The results indicated that the bursa of Fabricius, in relation to the other examined organs, was the most sensitive to this kind of stress. Histological changes of spleen and thymus were also observed, but less prominent except in chickens after more than 30 days of exposure to stress. According to our results, degree of histological changes of immune organs under the influence of sound stress depends on the length of exposure and age of chickens.

Sound Stress–Induced Long-Term Enhancement of Mechanical Hyperalgesia in Rats Is Maintained by Sympathoadrenal Catecholamines

Although stress plays an important role in chronic widespread pain syndromes, such as fibromyalgia, the underlying mechanism has remained elusive. We have recently demonstrated, in a model of chronic widespread pain, that prolonged enhancement of immune mediator hyperalgesia, induced by unpredictable sound stress, requires a contribution of both the sympathoadrenal (epinephrine) and the hypothalamic-pituitary adrenal (corticosterone) neuroendocrine stress axes. Because this stress protocol produced sustained elevation of plasma epinephrine, in the current study we tested the hypothesis that the sympathoadrenal axis also plays a role in maintenance of symptoms in this model of chronic widespread pain. After establishment, adrenal medullectomy abolished the enhancement of epinephrine-induced cutaneous and muscle hyperalgesia. Administration of stress levels of epinephrine to adrenal medullectomized rats reconstituted the pain phenotype. These observations suggest that the sympathoadrenal stress axis plays a major role in the induction as well as maintenance of stress-induced enhancement of mechanical hyperalgesia, mediated by prolonged elevation of circulating epinephrine. We present data showing mechanical hyperalgesia persisting for up to 28 days after exposure to sound stress, with evidence that the sympathoadrenal axis mediator epinephrine plays a major role. These findings could have clinical implications with regard to novel potential treatments for chronic widespread pain syndromes, such as fibromyalgia.

Activation of G i induces mechanical hyperalgesia poststress or inflammation

In studies of the role of primary afferent nociceptor plasticity in the transition from acute to chronic pain we recently reported that exposure to unpredictable sound stress or a prior inflammatory response induces long-term changes in the second messenger signaling pathway, in nociceptors, mediating inflammatory hyperalgesia; this change involves a switch from a G s-cAMP-PKA to a G i-PKCε signaling pathway. To more directly study the role of G i in mechanical hyperalgesia we evaluated the nociceptive effect of the G i activator, mastoparan. Intradermal injection of mastoparan in the rat hind paw induces dose-dependent (0.1 ng−1 μg) mechanical hyperalgesia. The highly selective inhibitors of G i, pertussis toxin, and of protein kinase C epsilon (PKCε), PKCεV 1-2, both markedly attenuate mastoparan-induced hyperalgesia in stressed rats but had no effect on mastoparan-induced hyperalgesia in unstressed rats. Similar effects were observed, at the site of nociceptive testing, after recovery from carrageenan-induced inflammation. These studies provide further confirmation for a switch to a G i-activated and PKCε-dependent signaling pathway in primary mechanical hyperalgesia, induced by stress or inflammation.

Anti-stress activity of hydro-alcoholic extract of Eugenia caryophyllus buds (clove)

Objective:The present study was undertaken to evaluate the anti-stress effect of the hydro-alcoholic extract of clove.Methodology:The anti-stress effect was evaluated on cold restraint induced gastric ulcers, sound stress induced biochemical changes and anoxic stress induced convulsions. Clove extract was administered orally at two different doses of 100 and 200 mg/kg. Zeetress, a known anti-stress formulation (14 mg/kg p.o) was used as the standard drug.Results:Both the doses of clove extract showed good anti-stress effect in all the tested models. The clove extract reduced the development of cold restraint induced gastric ulcers and prevented the biochemical changes induced by sound stress such as increase in plasma levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, glucose, cholesterol and corticosterone. Clove extract was also effective in increasing the latency of anoxic stress induced convulsions in mice.Conclusion:The hydro-alcoholic extract of clove at doses of 100 and 200 mg/kg orally possesses good anti-stress activity.

The influence of loud sound stress on expression of osmotic stress protein 94 in the murine inner ear

Osmotic stress protein 94 (OSP94), a member of the heat shock protein 110/SSE subfamily, is expressed in certain organs such as the kidney, testis, and brain where it can act as a molecular chaperon. In general, its alteration in expression is in response to hyper-ionic and osmotic stress as well as heat shock stress. Since many cells in the inner ear are involved in active ion transportation and are constantly exposed to two ionic different environments, we hypothesize that OSP94 may be expressed in the inner ear and its expression may be influenced by loud sound stress (LSS). With immunohistochemistry combined with confocal microscopy, immunoblotting, and reverse transcription polymerase chain reaction techniques, we found that OSP94 was widely expressed in various cells in the murine cochlea including the stria vascularis, the organ of Corti, the interdental cells, spiral ganglion cells, the spiral ligament, and Reissner's membrane. Under the unstressed condition, the transcription and protein level of OSP94 expression in the inner ear was quantitatively similar to that of the kidney. Furthermore, its expression in the inner ear by LSS from broadband noise at 117 dB/SPL was upregulated, but remained unchanged in the kidney. In particular, the upregulation of OSP94 in the cochlear lateral wall tissue was slowly elicited in a LSS time-dependent manner compared with the response of two other HSPs; HSP25 and HSP70 are considered to play a cytoprotective role under stressful conditions. Our results show that OSP94 is expressed in the inner ear and indicate this may be necessary for cells in a special ionic and osmotic environment such as endo-perilymphatic ion compartments. The organ-specific upregulation of OSP94 by acoustic overstimulation reveals that OSP94 in the murine inner ear is potentially important for cellular functional adaptation to LSS.

Stress-Induced Neurogenic Inflammation in Murine Skin Skews Dendritic Cells Towards Maturation and Migration: Key Role of Intercellular Adhesion Molecule-1/Leukocyte Function-Associated Antigen Interactions

The skin continuously serves as a biosensor of multiple exogenous stressors and integrates the resulting responses with an individual's central and peripheral endogenous response systems to perceived stress; it also acts to protect against external challenges such as wounding and infection. We have previously shown in mice that stress induces nerve growth factor- and substance P-dependent neurogenic inflammation, which includes the prominent clustering of MHC class II(+) cells. Because the contribution of dendritic cells (DCs) in response to stress is not well understood, we examined the role of DCs in neurogenic inflammation in murine skin using a well-established murine stress model. We show that sound stress increases the number of intradermal langerin(+) and CD11c(+) DCs and induces DC maturation, as indicated by the up-regulated expression of CD11c, MHC class II, and intercellular adhesion molecule-1 (ICAM-1). Blocking of ICAM-1/leukocyte function-associated antigen-1 interactions significantly abrogated the stress-induced numeric increase, maturation, and migration of dermal DCs in vivo and also reduced stress-induced keratinocyte apoptosis and endothelial cell expression of ICAM-1. In conclusion, stress exposure causes a state of immune alertness in the skin. Such adaptation processes may ensure protection from possible infections on wounding by stressors, such as attack by predators. However, present-day stressors have changed and such adaptations appear redundant and may overrun skin homeostasis by inducing immune dermatoses.

Sexual dimorphism in the effect of sound stress on neutrophil function

It has been hypothesized that stress contributes to the severity of inflammatory diseases. However, the mechanisms underlying this effect are incompletely understood. In this study we investigated the effects of sound stress on function of the polymorphonuclear neutrophil—immune cells that play key roles in both the acute and chronic inflammatory response. Specifically, we examined the effect of stress on the production of reactive oxygen species (ROS) and phagocytosis by rat neutrophils, and the role of sympathoadrenal stress axis in these effects. Since many inflammatory diseases exhibit sexual dimorphism, we also investigated the contribution of sex and gonadal hormones to the effects of stress on neutrophil function. Peripheral blood neutrophils were harvested from male and female rats exposed to intermittent sound stress (over 4 days). Stress suppressed ROS production in males (but not females) an effect that was eliminated in adrenal medullectomized males. Stress also suppressed neutrophil phagocytosis in males and females. Again, this effect was absent following adrenal medullectomy. To investigate the role of sex hormones in these sexual dimorphic responses to stress, rats were gonadectomized prepubertally and exposed to stress as adults. In gonadectomized males, stress produced an even larger decrease in ROS production, but had no effect on the stress-induced inhibition of phagocytosis. Gonadectomy prevented the stress-induced inhibition of neutrophil phagocytosis in females. These data indicate that the adrenal medulla, perhaps via release of epinephrine, suppresses neutrophil ROS production in males and phagocytosis in males and females.

Stress sensitive differentiation in expression of nerve fibers and antigen presenting cell and Substance P sensitive alteration of dendritic cell subpopulations in spleen

Substance P (SP) – a sensory neuropeptide – was revealed as an important stress mediator with its own stress axis in the skin. In this context, we were able to show, that stress‐dependent SP affects the migration of dendritic cell subpopulations to skin draining lymphnodes with subsequently altered T‐cell activation and disease activity in a mouse model for allergic dermatitis (AD). Here we postulate that stress‐dependent communication between nerve fibers and immune‐competent cells with effect on the course of inflammatory skin diseases can also occur in spleen. To address this question, AD was induced in C57BL/6 mice by double sensitization (i.p) and an intradermal challenge using chicken egg ovalbumin. Animals were additionally exposed to sound stress for 24 h prior to challenge. In this model, stress lead to a relative hyperinnervation of the immune‐competent areas of the spleen. At the same time, an increased number of antigen‐presenting cells (APC) could be observed in these areas and contacts between nerve fibers and APC were found. Substance P in vitro had the capacity to raise the number of antigen presenting cells in spleen and increased the number of CD4+ T‐cell‐stimulating CD4‐CD8‐ dendritic cells and further the number of CD25+ T‐regulatory cells. Further analysis of quality and function of neuro‐immune interactions in the spleen will reveal the role of the observed stress‐induced alterations in the spleen in atopic disease.