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Biomedical subjects

M Schedlowski

Publications and source records attributed to M Schedlowski.

At least 55 records · Page 3Linked to original sources
PubMed1998

A viro-psycho-immunological disease-model of a subtype affective disorder.

Borna Disease Virus (BDV) infections are widespread in animal species. This neurotropic, negative and single-stranded enveloped RNA virus spreads via axonal and transsynaptic pathways quite specifically into olfactoric and limbic structures. The symptoms in BDV-infected animals range from unapparent or subtle clinical manifestations to fatal neurological disorders. The severe and fulminant course of the infection, which is often accompanied by neurobehavioral and "emotional" disturbances, occurs sporadically and, at least in experimentally infected animals (rats), is thought to be mediated by immunopathology. Increases in serum-BDV antibodies have also been detected in neuropsychiatric patients. In addition, viral antigen and viral RNA have been observed in acutely ill major depressive patients, leading to the conclusion that BDV was causally related to psychiatric disorders, in particular to affective disorders. A number of studies have meanwhile furnished evidence of abnormal immune functions in mentally ill patients. In addition, stress has been shown to decrease immune responses to viral infections. On the basis of these findings it is hypothesized that human BDV infection represents a co-factor in the development or course of psychiatric diseases. Stress may cause immunosuppression and thus induce activation of persisting BDV in the limbic system, resulting in an inflammatory reaction of these structures. These neuropathological changes might influence the serotonergic or dopaminergic neurotransmitter systems. In addition, a specific affinity of BDV structural elements for aspartate and glutamate receptors in the hippocampal formation might directly induce an imbalance of these transmitter system interactions, causing affective and behavioral disturbances. The possible interactions between stress-induced immunosuppression, BDV infection and affective disorders in humans, and the theoretical and clinical aspects of this concept are discussed.

Animals↗
PubMed1998

Stress-induced endocrine and immunological changes in psoriasis patients and healthy controls. A preliminary study.

BACKGROUND: Clinical observations suggest that psychological stress can induce exacerbation of psoriasis. It is hypothesized that these stress effects on the course and outcome of psoriasis are caused by neuroendocrine modulation of immune functions. Therefore we investigated the cardiovascular, endocrine and immunological response to a laboratory stressor in psoriasis patients and healthy controls. METHODS: Untreated (n = 7) and PUVA-treated (n = 4) psoriatics and healthy controls (n = 7) were exposed to a brief laboratory stressor (public speaking and mental arithmetic). Heart rate and blood pressure, catecholamine, cortisol, and DHEA plasma concentration, as well as distribution of T and NK lymphocytes were analyzed before, immediately after and 1 h after stress exposure. RESULTS: Heart rate and blood pressure increased in all three groups during stress exposure with the most pronounced changes in PUVA-treated patients. Psoriasis patients displayed higher adrenaline values but diminished cortisol and DHEA plasma concentrations compared to controls. NK cell numbers (CD16+, CD56+), but not T lymphocyte subsets, increased immediately after stress exposure in untreated patients and controls. This effect was significantly diminished in PUVA-treated patients. CONCLUSIONS: The data of this pilot study indicate an enhanced stress-induced autonomic response and diminished pituitary-adrenal activity in psoriasis patients. PUVA treatment seems to interfere with the cardiovascular and NK cell response to acute psychological stress. Future studies will analyze the stress-induced neuroimmunological mechanisms in psoriatics in more detail.

Adult↗
PubMed1997

Adrenergic control of natural killer cell circulation and adhesion.

Natural killer (NK) cell circulation is subject to adrenergic regulation. Exactly how NK cells are released into the circulation is unknown. In an attempt to identify some of the mechanisms, the present report focuses on aspects of adhesion regulation of NK cells. Results demonstrate that interactions between NK and endothelial cells (EC) in vitro can be reduced by beta 2-adrenoceptor stimulation for as long as the receptor stimulation occurs. The level of soluble adhesion molecules (sICAM-1, sE-selectin, sVCAM-1) in vivo remained unchanged during adrenaline infusion. In vitro analyses further reveal the requirement for Ca2+/Mg2+ in NK-EC adhesion. Blocking studies indicate the involvement of several members of the beta 1(CD29)- and beta 2(CD18)-integrin family, reducing NK cell adhesion by 28 to 39%. Stimulation of beta 2-adrenoceptors in the presence of these blocking antibodies further reduced NK adhesion by an average of 22%. Analysis of NK cell adhesion to various extracellular matrix components demonstrates significant NK cell adhesion to fibronectin but much less to laminin or collagens I and IV. NK cell adhesion to fibronectin was reduced by 50% upon beta 2-adrenoceptor stimulation, independent of the VLA-4/VLA-5 binding site on fibronectin. Together these results contribute to understanding the influences of beta-adrenoceptor stimulation on NK cell circulation and adhesion.

Cell Adhesion↗
PubMed1997

Expression and in-vivo modulation of alpha- and beta-adrenoceptors on human natural killer (CD16+) cells.

Expression and in-vivo modulation of beta- and alpha-adrenoceptors on peripheral human natural killer (CD16+) cells was investigated. Ligand binding studies revealed that CD16+ lymphocytes express beta2, alpha1-, alpha2- but not beta1-adrenoceptors. Infusion of adrenaline, but not noradrenaline, significantly decreased beta2- and alpha1-adrenoceptor numbers on NK cells. Both catecholamines did not appreciably alter alpha2-adrenoceptor numbers. Additional analyses showed that adrenaline administration increases alpha2-adrenoceptor numbers on peripheral mononuclear blood cells (PBMC) and T-cell subsets (CD4+, CD8+) in contrast to decreased receptor numbers on CD16+ cells. These data demonstrate a specific effect of increasing levels of circulating catecholamines on beta2-adrenoceptors on NK cells.

Adrenergic Agonists↗
PubMed1996

Catecholamines modulate human NK cell circulation and function via spleen-independent beta 2-adrenergic mechanisms.

Increases in catecholamines have been shown to induce changes in migration of lymphocytes, in particular NK cells. To analyze the mechanisms of catecholamine-induced NK cell trafficking, normal healthy male human subjects and splenectomized individuals were infused with either adrenaline (0.10 microgram/kg/min), noradrenaline (0.15 microgram/kg/min), or NaCl i.v. for 20 min. Lymphocyte subsets (CD3+, CD4+, CD8+) transiently increased after administration of both catecholamines, with most pronounced increases (up to 600%) in NK cell numbers (CD16+ or CD56+) after infusion of adrenaline. These changes in NK cell numbers and function were accompanied neither by alterations in expression of adhesion molecules (CD11a), CD11b, CD31, CD43, CD44, CD62L) on NK cells nor by changes in plasma concentrations of soluble (s) adhesion molecules (sVCAM-1, sICAM-1, sE-selectin). Comparable increases in lymphocyte subsets were observed in splenectomized subjects, suggesting lymphocyte recruitment from other sources than the spleen. Furthermore, catecholamine-induced increases in lymphocyte subsets could be inhibited by pretreatment with the nonselective beta-adrenoceptor antagonist propranolol, but not by the beta1-selective antagonist bisoprolol. These data demonstrate that adrenaline and noradrenaline modulate the migratory capacity of human NK cells via spleen-independent beta 2-adrenoceptor mechanism.

Adrenergic beta-2 Receptor Antagonists↗
PubMed1996

Catecholamine-induced leukocytosis: early observations, current research, and future directions.

Recent studies demonstrate that acute psychological stress in man affects lymphocyte circulation. It has been suggested that catecholamines are responsible for these changes. The present review summarizes findings regarding catecholamine-induced lympho- and leukocytosis, starting with observations dating back to the beginning of this century. Particular attention is given to the mechanisms of this phenomenon and the potential site of origin of newly appearing leukocytes. Characteristically, two phases are recognized after catecholamine administration: a quick (<30 min) mobilization of lymphocytes, followed by an increase in granulocyte numbers with decreasing lymphocyte numbers. Many studies have shown that catecholamines predominantly affect natural killer (NK) cell and granulocyte circulation, whereas T- and B-cell numbers remain relatively unaffected. The changes in lymphocyte circulation seem to be mainly mediated via activation of beta2-adrenoceptors, whereas granulocyte increases involve alpha-adrenoceptor stimulation. Results further indicate that the marginal pool and the spleen are the major sources for freshly recruited lymphocytes, whereas granulocytes are predominantly released from the marginal pool and the lung. Results from acute psychological stress or physical exercise models corroborate the results obtained with catecholamine administration. Together, the data demonstrate that components of the innate immune system participate in the classical fight/flight response.

Acute Disease↗
PubMed1996

Epinephrine or norepinephrine fail to influence pituitary-adrenal secretion in man.

It is unknown whether plasma catecholamines have direct physiologic effects on pituitary-adrenocortical secretion in man. Therefore we investigated the effects of epinephrine and norepinephrine on plasma concentrations of adrenocorticotropin (ACTH), beta-endorphin and cortisol. Nineteen healthy male volunteers received infusions of either NaCl, epinephrine (0.10 micrograms/kg/min) or norepinephrine (0.15 micrograms/kg/min) for 20 minutes. 30 min before to 120 min after the infusion blood was continuously drawn to determine plasma levels of epinephrine, norepinephrine, and cortisol. In addition, ACTH and beta-endorphin plasma concentrations were analyzed at 6 time points before, during and after infusion. Infusion of catecholamines increased epinephrine and norepinephrine concentrations in physiological ranges as observed during intense psychological stress or exhausting physical exercise. However, these increases in catecholamine plasma levels neither affected concentrations of POMC-derived hormones nor plasma levels of cortisol. We conclude that in man, physiologic increases in circulating catecholamines have no influence on pituitary-adrenal hormone concentrations.

Adrenergic Agonists↗
PubMed1996

Modulation of the immunologic response to acute stress in humans by beta-blockade or benzodiazepines.

Acute stress evokes immediate responses in the cardiovascular endocrine, and immune systems. In particular, the number and activity of natural killer (NK) lymphocytes increase after stress. Here, we investigate the possibility to pharmacologically interfere with these stress-induced immunologic changes. Twenty-five healthy males were subjected to an acute stressor, a first-time tandem parachute jump. Subjects were randomly assigned to a beta-adrenoceptor antagonist (propranolol), a benzodiazepine (alprazolam), or placebo group. To analyze the role of the spleen in lymphocyte redistribution, splenectomized subjects performed a parachute jump. Propranolol, but no alprazolam, inhibited the heart rate increase during jumping. Increases in epinephrine and cortisol in the propranolol group were comparable to placebo, but were attenuated by alprazolam. The number and activity of NK cells significantly increased in the placebo group but not in the propranolol group immediately after stress. Alprazolam treatment did not alter the increase in NK cell numbers but did inhibit the increase in NK activity. In splenectomized subjects, NK cell numbers, but not NK activity, increased as in placebo subjects. We conclude that stress-induced changes in the immune system are controlled by beta-adrenergic mechanisms and only partly depend on the spleen; central interference with alprazolam differentially affects stress-induced changes in the NK cell compartment.

Adrenergic beta-Antagonists↗
PubMed1996

Excavation of caries lesions induces transient decrease of total salivary immunoglobulin A concentration.

Salivary immunoglobulin A (IgA) secreted by salivary glands is the predominant humoral factor of the local immune system in the oral cavity. Epidemiological studies emphasize the importance of salivary IgA in the protection from infections and caries. This study investigated how excavation of caries lesions affects total salivary IgA concentration. Fifteen patients were assigned to two sessions: the first session consisted of the excavation of a caries lesion. Thirty min before, during, directly after, and 30 min after the excavation, patients were asked for saliva samples. One wk later, a control session was performed on the same patients at the same time of the day, consisting of a dental inspection without any drilling. Marked, transient decreases were observed in concentration and secretion rate of total salivary immunoglobulin A during and immediately after caries excavation. Thirty min after caries excavation, immunoglobulin A concentrations returned to baseline. No differences were found between sessions with regard to saliva flow and cortisol concentration. It was concluded that transient decreases of total salivary immunoglobulin A concentrations are induced by excavation of caries lesions.

Adult↗
PubMed1996

Time kinetics of the endocrine response to acute psychological stress.

A first-time parachute jump was chosen as a model to evaluate the endocrine response to acute psychological stress. In 43 inexperienced tandem parachutists, blood was drawn continuously from 2 h before to 1 h after the jump and analyzed at 10-min intervals for plasma concentrations of epinephrine (E), norepinephrine (NE), cortisol, GH, PRL, and TSH. In addition, heart rate was recorded throughout the experiment. There was a significant increase in heart rate and E concentrations during the jump itself. NE, cortisol, GH, PRL, and TSH peaked with a latency of 10-20 min. Apart from cortisol and TSH concentrations, which were still elevated 1 h after the stress event, plasma levels of the other endocrine variables normalized within 1 h following the jump. Statistically significant cross-correlations could be observed between E and NE (r = 0.60, no time lag) and between E and PRL (r = 0.58, 10-min time lag) only. Even in a very homogenous group of subjects and under well-controlled conditions, endocrine responses to acute psychological stress show considerable variations.

Adult↗
PubMed1996

[Stress and the immune system].

Research in psychoneuroimmunology has demonstrated that biopsychosocial factors such as psychological stress can influence the immune system. Chronic stress has been associated with the suppression of the immune function. In contrast, acute psychological stressors and physical exercise have been shown to transiently enhance immune responses. These stress effects on immunity seem to be mediated via endocrine factors, since hormones, neurotransmitters, and neuropeptides can interact with cellular components of the immune system. In summary, experimental and clinical evidence suggests a functional relationship between stress, immunity, and diseases.

Animals↗
PubMed1996

Competition stress in soccer coaches increases salivary. Immunoglobin A and salivary cortisol concentrations.

The effect of acute psychological stress on salivary immunoglobulin A (sIgA) and salivary cortisol concentrations was studied in professional soccer coaches (n = 17) before, during, and after a match of their team. Saliva samples were collected at five time points (2 hours before the match, at the beginning of the match, during half time break, at the end of the match and one hour after the match) and analysed for sIgA and salivary cortisol together with the subjective rating of perceived psychophysiological arousal. In addition, control subjects (n = 8) were tested under resting conditions with identical procedures. Results show that soccer coaches rated themselves as more excited and tense during the match compared to time points before and after the match of their team. Furthermore, coaches revealed pronounced, transient increases in sIgA and salivary cortisol concentrations compared to control subjects. These data indicate, that acute psychological stress activates non-specific humoral immune functions.

Adult↗
PubMed1995

Beta-endorphin, but not substance-P, is increased by acute stress in humans.

The role of neuropeptides in the psychoneuroendocrinological stress response is largely unknown. In this study the effect of acute psychological stress on beta-endorphin and substance-P plasma concentrations was investigated and further the effect of different anxiety levels or control attributions on beta-endorphin or substance-P levels were determined. Blood samples were obtained from 47 inexperienced tandem-parachutists 2 h before, immediately after, and 1 h after a parachute jump and plasma concentrations of beta-endorphin and substance-P were analysed. Anxiety levels and control attributions were assessed by psychometric scales. Whereas substance-P concentrations seemed to be unaffected by the jump stress, there was a transient but significant increase in beta-endorphin levels immediately after jumping. However, subjects higher in state-anxiety at the point of jumping (exit) displayed higher substance-P values at all three time points compared to the "low-anxiety" jumpers. In addition, stress-induced beta-endorphin secretion was dependent on subjective control attributions.

Adult↗
PubMed1993

Changes of natural killer cells during acute psychological stress.

Emotional stress is often followed by increased susceptibility to infections. One major role in the immediate immune response to infection is played by natural killer (NK) cells. This study was designed to establish whether acute psychological stress influences cellular immune functions and to elucidate the role of endocrine parameters as potent mediators of stress induced alterations of the immune system. Forty-five first-time tandem parachutists were examined continuously for their plasma concentrations of cortisol and catecholamines from 120 min before to 60 min after jumping. Lymphocyte subsets, NK activity, and ADCC were determined 2 hr before, immediately after, and 1 hr after jumping. There was a significant increase in sympathetic-adrenal hormones during (adrenaline, noradrenaline) and shortly after jumping (cortisol). Lymphocyte subsets and the functional capacity of NK cells revealed an increase immediately after jumping followed by a decrease significantly below starting values 1 hr later. These changes were significantly correlated to plasma concentrations of noradrenaline. Thus, quick mobilization of NK cells is suggested as one major mechanism for this effective adaptation of the immune system to stress situations.

Acute Disease↗
PubMed1993

Catecholamines induce alterations of distribution and activity of human natural killer (NK) cells.

Catecholamines have been suggested to be responsible for altered cellular immunity after stress. This study was performed to determine the effects of adrenaline and noradrenaline on lymphocyte subpopulations and NK cell functions. Subjects were given a subcutaneous injection of either NaCl, adrenaline (5 micrograms/kg), or noradrenaline (10 micrograms/kg). Catecholamine concentrations, subsets of peripheral blood lymphocytes, NK activity, and antibody-dependent cellular cytotoxicity (ADCC) were analyzed before (baseline) and 5, 15, 30, 60, and 120 min after injection. There were no differences between groups in the distribution of CD2+ and CD8+ lymphocytes over time. However, CD3+ and CD4+ T cells decreased significantly 5 to 60 min after injection of adrenaline. In contrast, NK cell numbers (CD16+, CD56+) increased significantly 5 min after injection of adrenaline and noradrenaline, reached the highest values 15 to 30 min postinjection, and subsequently declined to baseline values 60 (noradrenaline) and 120 (adrenaline) min, respectively, after injection. Similar alterations for NK activity and ADCC were observed after administration of both catecholamines. These data suggest that both sympathetic-adrenal hormones are similarly potent modulators of natural immunity and provide further evidence that catecholamines might be responsible for the observed alterations in immune functions after phases of acute stress.

Adult↗
PubMed1993

Psychophysiological, neuroendocrine and cellular immune reactions under psychological stress.

Emotional stress is often followed by increased susceptibility to infections. Natural killer (NK) cells play a major role in the immediate immune response controlling this susceptibility. In this study on 45 first-time parachutists, it is demonstrated that highly controlled psychological stress increased psychophysiological variables, enhanced the secretion of sympathetic-adrenal hormones and also led to a significant increase of NK cells and their cytotoxic activity followed by a decrease below starting values. This immunological alteration is correlated with the secretion of noradrenaline during the emotional strain. Quick mobilization of these cytotoxic effector cells is suggested as a major mechanism for the effective adaptation of the immune system to stress situations.

Adult↗
PubMed1992

Acute psychological stress increases plasma levels of cortisol, prolactin and TSH.

The effects of acute stress during a parachute jump on hormonal responses were studied in 12 experienced and 11 inexperienced military parachutists. Each subject performed two jumps. Prior to and immediately after each jump blood samples were drawn and analysed for plasma levels of cortisol, prolactin, thyrotropin (TSH), somatotropin (STH), and luteinizing hormone (LH). While there was a significant increase in cortisol, prolactin and TSH levels after both jumps, no alterations could be observed in STH and LH levels. Stress-induced hormonal responses were not affected by jump experience. There was also no association between the endocrine variables and anxiety scores.

Acute Disease↗