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)

Frequent blood sampling from males rats was used to study hypothalamic-pituitary-adrenal (HPA) axis activation during arthritis and its association with diminished responses to acute psychological stress. In control rats, corticosterone release occurred in a series of 13 +/- 1 pulses per 24 h. Induction of arthritis by Mycobacterium-adjuvant injection initially increased the rate of hormone release within each pulse and, by day 14 postinjection, when hind-paw inflammation was established, caused a marked increase in pulse frequency to 22 +/- 1 per 24 h leading directly to elevated circulating corticosterone levels. In both control and adjuvant-treated rats, there was a marked response to a 10-min noise stress when the stimulus coincided with a rising or interpulse phase of the endogenous corticosterone rhythm. However, when the noise stress coincided with a falling phase of this rhythm, the response was greatly diminished. Since corticosterone pulse frequency was markedly increased and hence interpulse interval decreased by day 14, there was an increased probability of the noise stress occurring during the nonstress responsive falling phase of the corticosterone secretory cycle. As a result, the group mean response to noise stress was significantly smaller in the arthritic than the controls (70.2 +/- 9.2 versus 107.8 +/- 13.0 ng/ml, respectively). In contrast to the differential response to noise stress, all rats showed similar responses to the acute immunological challenge with i.v. lipopolysaccharide. Thus, altered basal pulse frequency is a major factor influencing HPA activation during acute psychological stress.
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PMID:Increased corticosterone pulse frequency during adjuvant-induced arthritis and its relationship to alterations in stress responsiveness. 1167 59

A previous exposure to an inflammatory reaction is known to increase or decrease the activation of the hypothalamic-pituitary-adrenal (HPA) axis induced by a psychological/physical stress. Beside HPA activation, the non- specific responses to these two kinds of stresses involve the immune system including the production of cytokines. Therefore, they could interfere in cytokine production. In order to test this hypothesis, female C3H mice were first injected i.p. with 5 microg of lipopolysaccharide (LPS) or not (C). Eight days later, half of them were submitted to a 4 h-restraint (R) applied during the nocturnal part of the dark-light cycle and sacrificed immediately after (groups LPS-R and C-R), while the non restrained mice stayed in their home cages (groups LPS-C and C-C). Restraint induced an increase in corticosterone production that was not altered by the previous administration of LPS. It had no effect on mitogen-induced lymphoproliferation. However, restraint induced an augmentation of plasma concentrations of interleukin (IL)-1 and IL-6 that was not observed in animals previously exposed to LPS. These results show that restraint, which represents a psychological stress is able to induce the production of plasma cytokines in mice. They also suggest that LPS may induce a long lasting suppression of plasma cytokines through mechanisms that remain to be elucidated.
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PMID:Suppression of restraint-induced plasma cytokines in mice pretreated with LPS. 1218 91

The subject of neuroinflammation is reviewed. In response to psychological stress or certain physical stressors, an inflammatory process may occur by release of neuropeptides, especially Substance P (SP), or other inflammatory mediators, from sensory nerves and the activation of mast cells or other inflammatory cells. Central neuropeptides, particularly corticosteroid releasing factor (CRF), and perhaps SP as well, initiate a systemic stress response by activation of neuroendocrinological pathways such as the sympathetic nervous system, hypothalamic pituitary axis, and the renin angiotensin system, with the release of the stress hormones (i.e., catecholamines, corticosteroids, growth hormone, glucagons, and renin). These, together with cytokines induced by stress, initiate the acute phase response (APR) and the induction of acute phase proteins, essential mediators of inflammation. Central nervous system norepinephrine may also induce the APR perhaps by macrophage activation and cytokine release. The increase in lipids with stress may also be a factor in macrophage activation, as may lipopolysaccharide which, I postulate, induces cytokines from hepatic Kupffer cells, subsequent to an enhanced absorption from the gastrointestinal tract during psychologic stress. The brain may initiate or inhibit the inflammatory process. The inflammatory response is contained within the psychological stress response which evolved later. Moreover, the same neuropeptides (i.e., CRF and possibly SP as well) mediate both stress and inflammation. Cytokines evoked by either a stress or inflammatory response may utilize similar somatosensory pathways to signal the brain. Other instances whereby stress may induce inflammatory changes are reviewed. I postulate that repeated episodes of acute or chronic psychogenic stress may produce chronic inflammatory changes which may result in atherosclerosis in the arteries or chronic inflammatory changes in other organs as well.
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PMID:Stress and the inflammatory response: a review of neurogenic inflammation. 1248 Apr 95

Previous studies have disagreed about whether prostaglandin EP1 or EP3 receptors are critical for producing febrile responses. We therefore injected lipopolysaccharide (LPS) at a variety doses (1 microg kg(-1)-1 mg kg(-1)) intraperitoneally (i.p.) into wild-type (WT) mice and mice lacking the EP1 or the EP3 receptors and measured changes in core temperature (Tc) by using telemetry. In WT mice, i.p. injection of LPS at 10 microg kg(-1) increased Tc about 1 degrees C, peaking 2 h after injection. At 100 microg kg(-1), LPS increased Tc, peaking 5-8 h after injection. LPS at 1 mg kg(-1) decreased Tc, reaching a nadir at 5-8 h after injection. In EP1 receptor knockout (KO) mice injected with 10 microg kg(-1) LPS, only the initial (< 40 min) increase in Tc was lacking; with 100 microg kg(-1) LPS the mice showed no febrile response. In EP3 receptor KO mice, LPS decreased Tc in a dose- and time-dependent manner. Furthermore, in EP3 receptor KO mice subcutaneous injection of turpentine did not induce fever. Both EP1 and EP3 receptor KO mice showed a normal circadian cycle of Tc and brief hyperthermia following psychological stress (cage-exchange stress and buddy-removal stress). The present study suggests that both the EP1 and the EP3 receptors play a role in fever induced by systemic inflammation but neither EP receptor is involved in the circadian rise in Tc or psychological stress-induced hyperthermia in mice.
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PMID:Characteristics of thermoregulatory and febrile responses in mice deficient in prostaglandin EP1 and EP3 receptors. 1283 30

The ability of postnatal testosterone propionate (TP) to masculinize both behaviour and gonadal cyclicity in the female rat is well documented. We have investigated whether postnatal androgen also has an organizational effect on another sexually dimorphic neuroendocrine system--the hypothalamo-pituitary-adrenal (HPA) axis. Female rats were exposed to a single injection of testosterone propionate (TP) or oil within 24 h of birth. As adults, rats were either ovariectomized and given 17beta-oestradiol replacement (OVXE2) or sham ovariectomized with cholesterol implants (SHOVX). An automated sampling system collected blood from unanaesthetized adult female rats every 10 min over a 24-h period, during a mild psychological stress (noise) and following an immunological lipopolysaccharide stress (LPS). Neonatal TP-treated SHOVX rats had a significant reduction in the number, height, frequency and amplitude of corticosterone pulses over the basal 24-h period, compared to both the neonatal oil-treated and TP-treated OVXE2 animals. The corticosterone response to both noise and LPS was also significantly decreased for the TP-treated SHOVX females. Three hours post-LPS administration, TP females had significantly lower values of paraventricular nucleus (PVN) corticotrophin releasing hormone (CRH), arginine vasopressin (AVP) and anterior pituitary proopiomelanocortin (POMC) mRNAs and greater PVN glucocorticoid receptor (GR) mRNA expression compared to the oil-treated controls. E2 replacement in adult TP rats normalized all the mRNA levels, except for PVN GR mRNA which did fall towards the levels of the oil-control animals. A single injection of TP within 24 h of birth disrupts the development of the characteristic female pattern of corticosterone secretion and the normal female HPA response to stress, resulting in a pattern similar to that seen in males. These effects can be reversed by E2 treatment in the adult TP female rat.
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PMID:Postnatal masculinization alters the HPA axis phenotype in the adult female rat. 1561 Oct 26

The bacterial endotoxin lipopolysaccharide (LPS) exerts strong effects on the immune-neuroendocrine network. On behaviour, LPS induces the symptoms of sickness behaviour. Otherwise, LPS challenge shares with psychological stress some common physiological adaptations. The proposal of this study was to analyse the effects of the LPS injection on the behavioural response in the shock-probe defensive burying test of two wild house mouse lines genetically selected for short (SAL) and long (LAL) latency to attack a conspecific. It is known that with previous exposure to stress, each of these lines exhibits behaviour in the burying test that is closely related to their different neuroendocrine patterns of response, with higher expression of burying in the SAL and immobility in the LAL mice. LPS (0.5 ml, 375 microg/Kg) or sterile saline (0.9%) was i.p. injected 3.5h before the beginning of the test. Non-injected mice were used as a general control of stress of handling and drug effect. The following behaviours were analyzed: defensive burying, immobility, rearing, grooming, exploration and jumping. The procedure of injection was found to be a stimulus that induced behavioural alterations in the SAL and LAL mice. Some behavioural changes induced by saline injection resembled that induced by LPS injection; in both lines an increase in immobility as well as a decrease in burying behaviour was observed. It is noteworthy that the LAL mice increased more their immobility than the SAL mice after saline or LPS injection, and the decrease in burying in the saline and LPS-injected mice was lower in the SAL than in the LAL mice. These results and others discussed in the text suggest that the active coping strategy of SAL mice and the passive coping strategy of the LAL mice, the hallmark of each line in the shock-probe burying test is present after psychological as well as LPS challenge exposure.
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PMID:Effects of LPS on the behavioural stress response of genetically selected aggressive and nonaggressive wild house mice. 1761 97

This study was aimed to test the hypothesis that noninvasive assessment of carotid plaques can be achieved by high-resolution micro-ultrasound imaging in apolipoprotein-E knockout (apoE-KO) mice. Forty-two male apoE-KO mice were fed a high-fat diet and atherosclerotic lesions in the left common carotid artery were induced by perivascular placement of constrictive collars. Eight weeks after surgery, all mice were divided into interventional group (n=21) which received mental stress stimulation and intraperitoneal injection of lipopolysaccharide, and control group (n=21) which received only 0.9% sodium chloride solution for 4 weeks. Plaque morphology and flow velocities were evaluated by micro-ultrasonography. The results showed that micro-ultrasound imaging and corresponding cross-sectional histopathology data revealed positive correlations for plaque area, intima-medial thickness (IMT), eccentric index (EI) and remodeling index (RI) (all p<0.05). Ultrasound-derived IMT, EI and RI in the ruptured plaques were significantly greater than those in the nonruptured plaques (all p<0.05). Maximal flow velocity (Vmax) was higher in the ruptured plaque sites compared with nonruptured plaques sites (p<0.001). Multivariate logistic regression analysis revealed that IMT and Vmax were independent predictors of plaque rupture. In conclusion, micro-ultrasound imaging provides a reliable approach to the noninvasive and quantitative assessment of carotid plaques in apoE-KO mice.
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PMID:Micro-ultrasound imaging assessment of carotid plaque characteristics in apolipoprotein-E knockout mice. 1787 80

Peripheral immune stimulation as well as certain types of psychological stress increases brain levels of inflammatory cytokines such as interleukin-1beta (IL-1beta), IL-6 and tumor necrosis factor alpha (TNFalpha). We have demonstrated that aged mice show greater increases in central inflammatory cytokines, as well as greater cognitive deficits, compared to adults in response to peripheral lipopolysaccharide (LPS) administration. Because aged mice are typically more sensitive to systemic stressors such as LPS, and certain psychological stressors induce physiological responses similar to those that follow LPS, we hypothesized that aged mice would be more sensitive to the physiological and cognitive effects of mild stress than adult mice. Here, adult (3-5 months) and aged (22-23 months) male BALB/c mice were trained in the Morris water maze for 5 days. Mice were then exposed to a mild restraint stress of 30 min before being tested in a working memory version of the water maze over a 3-day period. On day 4 mice were stressed and then killed for collection of blood and brain. In a separate group of animals, mice were killed immediately after one, two or three 30 min restraint sessions and blood was collected for peripheral corticosterone and cytokine protein measurement, and brains were dissected for central cytokine mRNA measurement. Stress disrupted spatial working memory in both adult and aged mice but to a much greater extent in the aged mice. In addition, aged mice showed an increase in stress-induced expression of hippocampal IL-1beta mRNA and MHC class II protein compared to non-stressed controls while expression in adult mice was unaffected by stress. These data show that aged mice are more sensitive to both the cognitive and inflammatory effects of mild stress than are adult mice and suggest a possible role for IL-1beta.
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PMID:Cognitive and neuroinflammatory consequences of mild repeated stress are exacerbated in aged mice. 1840 25

Emerging evidence suggests that acute psychological stress modulates inflammatory competence; however, not all findings are consistent. Gender is one factor that may impact magnitude of response. To explore this possibility, we examined the effects of acute mental stress on lipopolysaccharide-induced production of pro-inflammatory cytokines interleukin (IL)-1beta, IL-6, and tumor necrosis factor (TNF)-alpha among a relatively healthy sample of midlife men (n=28) and women (n=34). Blood samples for the assessment of cytokine production were drawn before, immediately after, and 30min following subjects' performance of an evaluative speech task. Relative to baseline evaluations, the speech stressor elicited a significant increase in stimulated production of all 3 pro-inflammatory cytokines, as measured 30min following the end of the task. There were no gender differences in the magnitude of this effect. However, men showed a significant decrease in cytokine production from before to immediately following the stressor, whereas women showed no change across this period. Menopausal status partially accounted for these gender differences, with post-menopausal women displaying greater increases in IL-6 and TNF-alpha production from baseline-to-post-task when compared to men. These data provide further evidence that acute psychological stress primes the immune system to mount larger inflammatory responses and initial support for gender differences in the patterning of stress-related cytokine activity. In addition, this study presents novel evidence that post-menopausal women may be particularly susceptible to stress-related inflammatory responses. The possibility that this contributes to the increased risk of inflammatory disease observed among older women warrants investigation.
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PMID:Gender differences in stimulated cytokine production following acute psychological stress. 1907 Jun 58

Recent studies from our laboratory indicate that psychological stress is a potent inducer of the anti-inflammatory cytokine interleukin (IL)-10, raising the possibility that the IL-10 family of cytokines may be key mediators of stress-induced immunosuppression. In this study we examined the impact of psychological stress (restraint stress) on expression of IL-10, and the novel IL-10 family members IL-19, IL-20 and IL-24 in mouse spleen following an in vivo challenge with lipopolysaccharide (LPS). We found that stressor exposure significantly augmented LPS-induced IL-10 expression. Similarly, IL-19 expression was induced by LPS, and this was significantly enhanced by restraint stress. In contrast, expression of IL-24 was not significantly altered by LPS or stress, and expression of IL-20 was largely not detectable in vivo in either saline or LPS-treated animals. Consistent with a role for sympathetic nervous system (SNS) activation in stress-induced immune regulation, the sympathetic neurotransmitter noradrenaline increased LPS-induced IL-10 and IL-19 expression in splenocytes and dendritic cells, and the ability of noradrenaline to induce expression of these cytokines was blocked by pre-treatment with the beta-adrenoceptor antagonist propranolol. Similarly, pre-treatment of mice with the peripherally acting beta-adrenoceptor antagonist nadolol completely blocked the stress-induced increase in IL-10 and IL-19 mRNA expression. Finally, pre-treatment with the benzodiazepine anxiolytic chlordiazepoxide prevented the stress-induced increase in IL-10 and IL-19 expression. Taken together, these data demonstrate that psychological stress induces expression of the IL-10 and its homolog IL-19 via activation of beta-adrenoceptors, and the ability of stress to induce these cytokines is prevented by treatment with the anxiolytic chlordiazepoxide. The findings suggest that stress enhances the production of immunosuppressive cytokines, which may impact on stress-related disease processes.
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PMID:Psychological stress increases expression of IL-10 and its homolog IL-19 via beta-adrenoceptor activation: reversal by the anxiolytic chlordiazepoxide. 1915 73


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