Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypothalamic-pituitary-adrenocortical hormones, i.e. prolactin (PRL), human growth hormone (hGH), thyroid stimulating hormone (TSH), and Cortisol and plasma levels of cytokines, i.e. tumor necrosis factor-alpha (TNF-alpha), interleukin 1 beta (IL-1 beta), and interleukin-6 (IL-6), were assessed in 27 patients with persistent vegetative state (PVS) and in 16 outcome patients. In comparison with normal parameters, plasma levels of TSH were not significantly altered, while elevated basal hGH concentrations in 48.1% of PVS subjects and depressed cortisol levels in all PVS individuals and in patients who emerged from coma (outcome patients), respectively, were observed. In addition, higher TNF-alpha plasma levels in PVS subjects than in outcome patients and in healthy donors were found, while IL-1 beta plasma levels were elevated in both groups of patients in comparison with healthy controls. Of interest, in 55% PVS male patients hyperprolactinemia was observed, whereas in outcome patients more than six months these values were within normal range. In four patients, who emerged from coma in the course of this study, prolactin plasma levels were followed-up and increased basal values progressively fell to normal range within six months.
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PMID:Evaluation of hypothalamic-pituitary-adrenocortical hormones and inflammatory cytokines in patients with persistent vegetative state. 980 31

There is evidence that inflammatory responses have been induced in the tissues and body fluids of many SIDS infants. We suggested that some of these deaths are due to uncontrolled inflammatory responses to infectious agents and possibly cigarette smoke. The majority of SIDS deaths occur during the 2-4 month age range when infants have decreasing levels of maternal antibodies to infectious agents. Most deaths occur during the early hours of the morning. Adults are more susceptible to inflammatory responses at night due to lower levels of cortisol associated with circadian rhythm patterns. Infants develop these patterns between the ages of 7 weeks and 4 months, at which time their night-time cortisol levels drop dramatically. The objective of this study was to use an in vitro model system to assess the effects of different cortisol levels on proinflammatory cytokine production in response to the staphylococcal toxic shock syndrome toxin-1 (TSST-1) which has been identified in a significant number of SIDS infants. Levels of cortisol present in infants at night and during the day before and after the development of the circadian rhythm pattern were examined. Human buffy coats (n = 9) were stimulated with TSST-1 and responses assessed over 72 hours by a bioassay for tumour necrosis factor-alpha (TNF-alpha) and an enzyme linked immunosorbent assay (ELISA) for interleukin-6 (IL-6). Cortisol levels present in an infant at night after development of circadian rhythm (< or = 5 microg dl(-1)), did not significantly increase or decrease production of either TNF-alpha or IL-6. Concentrations of cortisol greater than 5 microg dl(-1) usually found in infants during the day or at night prior to the physiological change significantly decreased production of TNF-alpha at 12 hours and of IL-6 at 12 and 16 hours. Only cortisol levels greater than 5 microg dl(-1) significantly decreased production of the pro-inflammatory cytokines by human buffy coats stimulated with TSST-1. If the switch to the circadian rhythm pattern occurs in an infant when maternal antibodies are still present or after they have developed their own active immunity, the infant could neutralise common viruses, toxins or bacteria: however, if this switch occurs in an infant when antibody levels are low, this could be a window of vulnerability during which infants are at an increased risk of death if uncontrolled inflammatory responses are induced by infectious agents or their products.
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PMID:Cortisol levels and control of inflammatory responses to toxic shock syndrome toxin-1 (TSST-1): the prevalence of night-time deaths in sudden infant death syndrome (SIDS). 1044 9

Within the last few years, increasing evidence of relative adrenal insufficiency in septic shock evoked a reassessment of hydrocortisone therapy. To evaluate the effects of hydrocortisone on the balance between proinflammatory and antiinflammation, 40 patients with septic shock were randomized in a double-blind crossover study to receive either the first 100 mg of hydrocortisone as a loading dose and 10 mg per hour until Day 3 (n = 20) or placebo (n = 20), followed by the opposite medication until Day 6. Hydrocortisone infusion induced an increase of mean arterial pressure, systemic vascular resistance, and a decline of heart rate, cardiac index, and norepinephrine requirement. A reduction of plasma nitrite/nitrate indicated inhibition of nitric oxide formation and correlated with a reduction of vasopressor support. The inflammatory response (interleukin-6 and interleukin-8), endothelial (soluble E-selectin) and neutrophil activation (expression of CD11b, CD64), and antiinflammatory response (soluble tumor necrosis factor receptors I and II and interleukin-10) were attenuated. In peripheral blood monocytes, human leukocyte antigen-DR expression was only slightly depressed, whereas in vitro phagocytosis and the monocyte-activating cytokine interleukin-12 increased. Hydrocortisone withdrawal induced hemodynamic and immunologic rebound effects. In conclusion, hydrocortisone therapy restored hemodynamic stability and differentially modulated the immunologic response to stress in a way of antiinflammation rather than immunosuppression.
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PMID:Immunologic and hemodynamic effects of "low-dose" hydrocortisone in septic shock: a double-blind, randomized, placebo-controlled, crossover study. 1258 9

Altered hypothalamo-pituitary-adrenal axis was reported in stroke patients; however, mechanisms responsible for this phenomenon are barely understood. Acute cerebral ischemia triggers interleukin-6 (IL-6) release into blood. Circulating IL-6 can stimulate hypothalamo-pituitary-adrenal axis. The goal of our study was to assess a relationship between serum IL-6 and cortisol in acute ischemic stroke. Twenty two patients with ischemic stroke and 17 controls were included. Serum samples were collected on the 2nd day of stroke at 6:00, 10:00 18:00, 22:00 h and at the same time points in control group. Cytokines and cortisol levels were measured using ELISA method. Serum IL-6 and cortisol levels were higher in stroke patients than in controls. Cortisol displayed diurnal variations in both stroke patients and controls. In contrast with control subjects, serum IL-6 levels did not display diurnal variations in stroke patients. In stroke patients, but not in controls, IL-6 level correlated significantly with cortisol level and morning serum IL-6 level independently predicted evening/night cortisol level. In conclusion, brain ischemia could stimulate IL-6 release in blood and in this way modulate hypothalamo-pituitary-adrenal axis.
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PMID:Serum interleukin-6 predicts cortisol release in acute stroke patients. 1505 41

The endocrine and immune changes associated with surgery are well documented, but the interaction between them has not been fully evaluated. We, therefore, investigated the possible effects of laparascopic cholecystectomy operation on C-reactive protein, hormones, and cytokines. Thirty-five patients were enrolled in the study (26 females and 9 males, aged 42.4 +/- 16.9 yr, who were admitted to General Surgery Clinic for laparascopic cholecystectomy). Serum C-reactive protein, cortisol, thyroid stimulating hormone, free tri-iodothyronine, free thyroxine, tumor necrosis factor-alpha, interleukin-1beta, soluble interleukin-2 receptor, interleukin-6, and interleukin-8 levels were evaluated 6 h before and after the operation. Postoperative cortisol (p=0.02), TSH (p=0.034), tumor necrosis factor-alpha (p=0.003), soluble interleukin-2 receptor (p=0.004) were found to be significantly higher than their corresponding preoperative levels. However, postoperative serum free thyroxine (p=0.011), and free tri-iodothyronine levels (p=0.001) were decreased when compared with preoperative levels, respectively. No significant difference was observed in C-reactive protein, interleukin-1beta, interleukin-6, and interleukin-8 levels. C-rective protein levels did not change in the early period of the surgical stress. Cytokine responses observed in the early period were found to be conflicting. Cortisol is an important marker of surgical stress which also has close relationship with thyroid functions.
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PMID:The effects of laparascopic cholecystectomy operation on C-reactive protein, hormones, and cytokines. 1512 3

Both exhaustive physical exertion and starvation have been reported to induce depression of immune function. The aim of the present study was to investigate the inflammatory environment and state of activation and mediator-producing potential of circulating leukocytes during prolonged physical activity with concomitant energy and sleep deprivation. Eight well-trained males were studied during 7 days of semi-continuous physical activity. Sleep was restricted to about 1 h/24 h, energy intake to 1.5- 3.0 MJ/24 h. Blood was drawn at 07.00 A.M.: on days 0, 2, 4, and 7. Plasma levels of inflammation markers were measured. The response of circulating leukocytes to lipopolysaccharide (LPS; 1 microg mL(-1)), and the effect of added hydrocortisone (10 and 100 nmol L(-1)), were measured in the supernatant after 3 h of incubation in an ex vivo whole blood model. Activation of leukocytes steadily increased as measured by plasma matrix metalloproteinase-9, tumour necrosis factor-alpha, interleukin-1beta, and interleukin-6. Inhibitors of systemic inflammation were either unaltered (tissue inhibitor of matrix metalloproteinase-1) or elevated (plasma interleukin-1 receptor antagonist). Cortisol levels increased on days 2 and 4, but thereafter reverted to baseline values. The leukocytes responded to LPS activation with increasing release of inflammatory cytokines throughout the study period. The anti-inflammatory potency of hydrocortisone decreased. Prolonged multifactorial stress thus activated circulating immune cells and primed them for an increased response to a subsequent microbial challenge.
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PMID:Seven days' around the clock exhaustive physical exertion combined with energy depletion and sleep deprivation primes circulating leukocytes. 1650 59

The inflammatory responsive cytokine interleukin-6 (IL-6) helps regulate immune responses to exercise. Evidence suggests that increases in IL-6 are related to exercise duration and intensity. However, the moderating effect of sex and underlying mediators have received limited attention. We compared plasma IL-6 responses to two cycling tasks with a resting control in young male (n = 12) and female (n = 12) recreationally active adults. Both 45 min tasks comprised an incremental test, either maximal or submaximal, followed by steady-state exercise at 55% peak power output. Interleukin-6 was elevated above baseline immediately after the maximal but not the submaximal task. Compared with the control condition, IL-6 was increased at 30 and 60 min after both exercise tasks. The IL-6 response was greater in women than men at 60 min after maximal exercise. Cortisol increased in both tasks compared with the control condition, the increase being greater after maximal than submaximal exercise. No associations were found between IL-6 responses and cortisol, heart rate, fitness or body mass index. The results show that 45 min of moderate-intensity exercise can increase IL-6 and suggest that the inclusion of maximal effort may accelerate this response. The finding that women showed a greater IL-6 response to maximal exercise may reflect a gender dimorphism in the immune response to stress.
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PMID:Individual differences in the interleukin-6 response to maximal and submaximal exercise tasks. 1681 80

Polymyalgia rheumatica (PMR) usually exhibits a good clinical response to glucocorticoid (GC) treatment, but early clinical symptoms may create some difficulties in the differential diagnosis with elderly onset rheumatoid arthritis (EORA), particularly in patients complaining of shoulder and pelvic girdle involvement at onset (PMR-like clinical onset) (EORA/PMR). Since neuroendocrine mechanisms seem to play a pathogenetic role in these clinical conditions, the aim of this study was to evaluate hormone and cytokine responsiveness to GC treatment in these patients. Cortisol (CO), dehydroepiandrosterone sulphate (DHEAS), 17-OH-progesterone (PRG), interleukin-1 receptor antagonist (IL-1Ra), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) were evaluated at base line, and 1 month after GC treatment (prednisone 10 mg/day), in 14 PMR, 11 EORA/PMR, and 13 EORA patients (mean age 73 +/- 5 years, +/- SD, mean disease duration 3 +/- 2 months, +/- SD). No patient was taking GCs or immunosuppressive agents at base line. Following GC treatment, CO, DHEAS, and PRG decreased significantly in both PMR and EORA/PMR patients (P < 0.05), but not in EORA patients. On the contrary, IL-1Ra was significantly increased in both PMR and EORA/PMR patients (P < 0.05). IL-6 and TNF-alpha serum levels were significantly decreased in all groups of patients (P < 0.05). In conclusion, PMR and EORA/PMR seem to exhibit similar hormonal variations after GC administration, when compared to EORA patients. These differences suggest a deficient function of the hypothalamic-pituitary-adrenal (HPA) axis in PMR and EORA/PMR patients, with a related higher responsiveness to GC treatment. Interestingly, in PMR and EORA/PMR patients, GC treatment was found to downregulate PRG serum levels.
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PMID:Glucocorticoid effects on adrenal steroids and cytokine responsiveness in polymyalgia rheumatica and elderly onset rheumatoid arthritis. 1685 58

Tuberculosis (TB) may be regarded as a disease in which the immune response to Mycobacterium tuberculosis, its etiologic agent, is engaged both in protection and pathology. Different T-lymphocyte subsets are involved in the immune response against M. tuberculosis, but production of interferon-gamma (IFN-gamma) by T cells seems to be fundamental for disease control. Th1-type cytokine responses predominate in patients with mild or moderate forms of pulmonary TB, whereas the production of Th2-type cytokines prevails in the severe disease. Since the immune response fails to definitely eradicate the pathogen, a chronic infection is established, and it is likely that a broad range of regulatory mechanisms operate in this situation. Cytokines released during the course of an immune response activate the hypothalamus-pituitary-adrenal axis leading to the production of glucocorticoids and dehydroepiandrosterone (DHEA), with known immunomodulatory effects. TB patients exhibit increased concentrations of interleukin-6 and cortisol in plasma, reduced DHEA and testosterone levels, together with remarkably increased growth hormone concentrations that were not accompanied by an expected raise in insulin-like growth factor-1. Significant increases in estradiol, prolactin, and thyroid hormone concentrations were also detected in patients. Cortisol inhibits the mycobacterial antigen-driven proliferation and IFN-gamma production, whereas DHEA suppresses transforming growth factor beta production by lymphoid cells from TB patients with advanced disease. Furthermore, supernatants from cultures of M. tuberculosis-stimulated mononuclear cells of TB patients inhibit DHEA secretion by a human adrenal cell line. This type of immuno-endocrine interactions may affect the control of tissue damage and the development of protective immune responses, partly accounting for disease aggravation.
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PMID:The immuno-endocrine component in the pathogenesis of tuberculosis. 1763 94

The effect of hydrocortisone on the production of interleukin-6 (IL-6) in human peripheral blood mononuclear cells was studied. Using our newly developed radioimmunoassay system for IL-6 of which specificity, reproducibility, sensitivity and usefulness have been demonstrated. IL-6 production in peripheral blood mononuclear cells of ten normal subjects revealed that in lipopolysaccharide (LPS, 10mug/ml)-stimulation, the mean +/- SD of IL-6 was 2.71 +/- 0.85 ng/ml. No detectable amount of IL-6 was observed in the absence of LPS and in the presence of hydrocortisone alone. Hydrocortisone (10(-10) M to 10(-3) M) inhibited LPS-stimulated IL-6 production in a dose-dependent manner. However, there was a wide variation in the response to hydrocortisone, namely, ranging from steroid-sensitive to steroid-resistant. Based on the concentration required to inhibit 50% of LPS-stimulated IL-6 production, three of ten subjects were at 10(-6) M, three at 10(-5) M and the rest at 10(-4) M, respectively. The dramatic anti-inflammatory and immunosuppressive effects of glucocorticosteroids can be life-saving in autoimmune diseases. The present findings suggested that there existed the differences in susceptibility to glucocorticosteroids even among normal subjects, providing some implications for the drug treatment, and also gave further evidence that there may exist an immunoregulatory feedback circuit between the immune and neuroendocrine systems.
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PMID:Effect of hydrocortisone on interleukin-6 production in human ,peripheral blood rnononuclear ceils. 1847 34


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