Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to compare the febrile responses of Fischer 344 rats of different ages [young (3-5 mo), mature (12-15 mo), and aged (24-27 mo; n = 8)] to two psychological stress paradigms, cage switch and exposure to an open field, as well as to injection of lipopolysaccharide (LPS). In addition, the cytokines tumor necrosis factor-alpha (TNF) and interleukin-6 were also measured in the plasma of these rats at 90 min postinjection with LPS. There was no significant difference among groups in febrile responses to switching their cages. Exposure to an open field for 30 min resulted in a smaller rise in temperature in the aged rats (0.62 degree C) than in the young rats (1.26 degrees C). This difference disappeared if rats were exposed to an open field for 60 min. Injection of LPS led to fevers that developed at a slower rate in aged rats than in the mature groups. The peak fevers, however, were not different. The activity of interleukin-6 90 min after injection of LPS was higher in aged rats (297,858 U/ml) than in young (17,462 U/ml) and mature rats (28,819 U/ml). TNF levels were also higher in aged rats (16,380 U/ml) compared with young (574 U/ml) and mature rats (36 U/ml). We conclude that although the magnitude of the febrile response is not different among rats of different ages, the rise in body temperature occurs slower in aged rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fever, tumor necrosis factor, and interleukin-6 in young, mature, and aged Fischer 344 rats. 153 27

Psychological stress (e.g., exposure to a novel environment) causes a rapid rise in body temperature in rats. In this study, we examined the roles of physical activity and the immune cytokine tumor necrosis factor or cachectin (TNF) in this temperature change. The elevation in temperature of rats exposed to cage-switch stress during the day correlated poorly with the increase in activity (r = 0.07; P = 0.84) and, during cage switch at night, correlated negatively (r = 0.64; P = 0.04). TNF was not detected in the plasma or cerebrospinal fluid of rats after exposure to open-field stress. However, the injection of antiserum against TNF 3.5 h before exposure to the stress of being in an open field resulted in a significantly greater hyperthermia than was seen in the control serum-injected rats (1.38 +/- 0.11 vs. 0.79 +/- 0.14 degrees C; P = 0.002). The peak temperature change after cage-switch stress was similarly increased in rats that had been injected with anti-TNF (0.82 +/- 0.08 vs. 0.50 +/- 0.08 degrees C; P = 0.016). This enhanced hyperthermia is similar to the excessively high fever that occurs during the later phase of lipopolysaccharide fever in animals that have been injected with antiserum against TNF. These data support the hypotheses that stress hyperthermia is a true fever and that TNF is an endogenous antipyretic, limiting the magnitude of this fever.
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PMID:Antiserum against tumor necrosis factor increases stress hyperthermia in rats. 231 7

The purpose of this study was to determine the effects of a particular psychological stress, exposure to an open-field, on plasma IL-6 activity in rats. Plasma IL-6 activity was 40.6 +/- 7.2 units/ml in control rats, 105 +/- 6.8 units/ml after 30 minutes exposure to an open-field, and 221 +/- 17 units/ml after 60 minutes of exposure (p = 0.0003). There was a positive correlation (r = .71, p = 0.043) between the change in plasma IL-6 activity and body temperature. However, we conclude, based on earlier data relating plasma IL-6 activity to body temperature changes following injection of lipopolysaccharide, that the plasma levels of IL-6 following exposure to an open-field are not high enough to account for the rise in body temperature observed in rats during this stress. In conclusion, these experiments indicate that exposure to psychological stress can elevate the plasma concentration of IL-6, a known mediator of the acute phase response.
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PMID:The effects of psychological stress on plasma interleukin-6 activity in rats. 238 52

There is evidence that psychological stress adversely affects the immune system. We have investigated the effects of such stress, caused by caring for a relative with Alzheimer's disease, on wound healing. We studied 13 women caring for demented relatives (mean age 62.3 [SE 2.3] years) and 13 controls matched for age (60.4 [2.8] years) and family income. All subjects underwent a 3.5 mm punch biopsy wound. Healing was assessed by photography of the wound and the response to hydrogen peroxide (healing was defined as no foaming). Wound healing took significantly longer in caregivers than in controls (48.7 [2.9] vs 39.3 [3.0] days, p < 0.05). Peripheral-blood leucocytes from caregivers produced significantly less interleukin-1 beta mRNA in response to lipopolysaccharide stimulation than did controls' cells. Stress-related defects in wound repair could have important clinical implications, for instance for recovery from surgery.
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PMID:Slowing of wound healing by psychological stress. 853 57

Using an isolated perfused rat liver (IPRL) preparation, we assessed whether corticosterone may contribute to the rise in tumor necrosis factor (TNF) and interleukin-6 (IL-6) in rats after injection with lipopolysaccharide (LPS) or exposure to psychological stress. Intravenous infusion of LPS into the IPRL led to dose-dependent increases in TNF and IL-6 concentrations in the effluent. Anisomycin, a protein synthesis inhibitor, completely blocked the rise in TNF and IL-6 concentration in the IPRL effluent, supporting the hypothesis that the synthesis (or release) of these cytokines was dependent on protein synthesis. Intravenous infusion of corticosterone at nonstressed (35 ng/ml) and stressed levels (350 ng/ml) increased TNF and/or IL-6 release. However, when LPS was combined with corticosterone, the lower dose of corticosterone facilitated the release of cytokines, whereas the higher dose of corticosterone suppressed the release of cytokines. We then showed that isolated Kupffer cells were capable of significant TNF and IL-6 production and that corticosterone decreased LPS-induced cytokine production in these cells. Our data support the hypothesis that the liver is an important source of circulating cytokines in response to LPS. In addition, although in vitro data generally support the hypothesis that corticosterone suppresses the production of cytokines, our in situ data support the hypothesis that physiological levels of corticosterone cause an increase in TNF and IL-6.
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PMID:Role of corticosterone in TNF and IL-6 production in isolated perfused rat liver. 790 Sep 13

Glucocorticoids exert negative feedback in the anterior hypothalamus (AH) during lipopolysaccharide (LPS)-induced fevers, but the central location of their negative feedback during psychological stress-induced fever has not been determined. To confirm that glucocorticoid modulation of LPS fever occurs in the AH, adrenalectomized animals were injected intrahypothalamically with either 0.25 ng of corticosterone or vehicle followed by 50 micrograms/kg LPS intraperitoneally. Animals pretreated with corticosterone developed significantly smaller fevers (P = 0.007) than animals given vehicle. To determine if glucocorticoid modulation during psychological stress-induced fever may occur in the hippocampus, the fornix was transected to block hippocampal communication with the AH. This resulted in significantly larger psychological stress-induced fevers (P = 0.02) compared with sham-operated animals. There were no differences between these groups for LPS-induced fevers (P = 0.92). To determine where in the hippocampus glucocorticoids might exert their negative feedback during psychological stress, rats were microinjected with either 1 ng RU-38486 (a type II glucocorticoid receptor antagonist) or vehicle into the dentate gyrus prior to exposure to the open field. There were no differences between the psychological stress-induced fevers of the RU-38486- and vehicle-injected groups, supporting the hypothesis that these fevers are modulated elsewhere in the hippocampus. Our data support the hypothesis that glucocorticoids modulate LPS-induced fever in the AH and do not involve the hippocampus, and that psychological stress-induced fevers are modulated by neural connections between the hippocampus and the hypothalamus. The precise sites of action of glucocorticoid negative feedback on stress-induced fevers in the hippocampus (or other brain regions) are not yet known.
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PMID:The CNS site of glucocorticoid negative feedback during LPS- and psychological stress-induced fevers. 885 98

Old rats may show blunted fever or hypothermia after injection of lipopolysaccharide (LPS), a fever-producing agent, and have a reduced body temperature (Tb) rise in response to psychological stress. These results may partly be a consequence of aging per se, partly a sex difference, and partly an effect of differences in types and doses of pyrogen. Here we tested age and gender differences in Tb responses to 30-min exposure to a novel environment and to injection of several doses of LPS. There were age-related reductions in novelty-induced hyperthermia, and some old rats even became hypothermic. Sensitivity to the pyrogenic activity of LPS and to the toxic effects of endotoxin (manifested by hypothermia) both increased in aged female rats. A major finding was that there were no correlations between age-related changes in Tb in response to novelty and to LPS injection. Tb responses in aged rats were variable; in each situation, there were old rats whose Tb rose as high as did younger ones. We did not observe significant gender differences in response either to novelty or to LPS in young or old rats.
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PMID:Individual differences in response to LPS and psychological stress in aged rats. 914 27

Inability to mount a suitable glucocorticoid response to a stressor can be life-threatening. Rats with hind-paw inflammation, associated with the development of adjuvant-induced arthritis (AA), are unable to mount a hypothalamo-pituitary-adrenal (HPA) axis response to acute stress. In the present study we have compared the effects of acute psychological stress (noise) and acute immunological challenge (lipopolysaccharide [LPS] injection), on the activation of the HPA axis in rats with the chronic inflammatory stress of AA. We conclude that the increase in HPA axis activity in AA is principally due to an increase in corticosterone pulse frequency and not to any alteration in pulse magnitude. The lack of response to acute stress can be accounted for by the increase in pulse frequency and the associated refractory period following each pulse, producing dramatic but specific changes in basal HPA function. These changes may account for the loss of responsiveness to acute stress, but not to acute immunological challenge, because the HPA axis is able to respond to LPS in male rats with AA. However, there appears to be an impaired adrenal responsiveness in female rats with AA that is not inherent, but occurs as a consequence of the development of inflammation.
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PMID:Differential effects of psychological and immunological challenge on the hypothalamo-pituitary-adrenal axis function in adjuvant-induced arthritis. 1041 92

Endomorphin (EM)-1 and EM-2 are opioid tetrapeptides recently located in the central nervous system and immune tissues with high selectivity and affinity for the mu-opioid receptor. Intracerebroventricular (i.c.v.) administration of morphine stimulates the hypothalamo-pituitary-adrenal (HPA) axis. The present study investigated the effect of centrally administered EM-1 and EM-2 on HPA axis activation. Rats received a single i.c.v. injection of either EM-1 (0.1, 1.0, 10 microg), EM-2 (10 microg), morphine (10 microg), or vehicle (0.9% saline). Blood samples for plasma corticosterone determinations were taken immediately prior to i.c.v. administration and at various time points up to 4 h post-injection. Trunk blood, brains and pituitaries were collected at 4 h. Intracerebroventricular morphine increased plasma corticosterone levels within 30 min, whereas EM-1 and EM-2 were without effect. In addition, pre-treatment of i.c.v. EM-1 did not block the rise in corticosterone after morphine. Corticotrophin-releasing factor (CRF) mRNA and arginine vasopressin (AVP) mRNA in the paraventricular nucleus (PVN) and POMC mRNA in the anterior pituitary were found to be unaffected by either morphine or endomorphins. Since release of other opioids are elevated in response to acute stress, we exposed rats to a range of stressors to determine whether plasma EM-1 and EM-2 can be stimulated by HPA axis activation. Plasma corticosterone, ACTH and beta-endorphin were elevated following acute restraint stress, but concentrations of plasma EM-1-immunoreactivity (ir) and EM-2-ir did not change significantly. Corticosterone, ACTH and beta-endorphin were further elevated in adjuvant-induced arthritis (AA) rats by a single injection of lipopolysaccharide (LPS), but not by restraint stress. In conclusion, neither EM-1 or EM-2 appear to influence the regulation of the HPA axis. These data suggest that endomorphins may be acting on a different subset of the mu-opioid receptor than morphine. The failure to induce changes in plasma EM-ir in response to the chronic inflammatory stress of AA, the acute immunological stress of LPS, or the psychological stress of restraint, argues against an important role for endomorphins in mediating HPA axis activity.
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PMID:Endomorphins and activation of the hypothalamo-pituitary-adrenal axis. 1125 Jun 60

We have studied the following stress model: the tension caused by sitting for the theoretical part of the driving license examination. Volunteers were investigated twice, after their driving license examination and after a (stress-free) control session. The effects of the stress were investigated by studying the blood picture (differential counts), serum concentration of cortisol, and cytokine production in stimulated blood cells. Relationships between the subjective perception of stress and the physiological reaction were also investigated. This stress induced significant increase in the concentrations of cortisol and hemoglobin, and in the values of hematocrit and MCV, and in the lipopolysaccharide-induced release of IL-1beta and -6. The subjective feelings of irritability and wakefulness were also significantly higher after the exam. A significant relationship was found between the changes in the stimulated production of IL-1beta and irritability. The responsiveness to psychological stress might be influenced by the temporary mood of the subjects.
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PMID:The driving license examination as a stress model: effects on blood picture, serum cortisol and the production of interleukins in man. 1126 76


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