Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Metallothionein (MT), a low molecular-weight, cysteine-rich, metal-binding protein, is induced by many environmental factors and a variety of stimuli. Bacterial endotoxin (lipopolysaccharide, LPS) injection is experimentally used to produce acute stress and is an effective inducer of hepatic MT. However, the mechanism of LPS induction of MT is not known. In the present studies, we used two substrains of mice, differing in their production of cytokines after LPS administration, to test the hypothesis that MT induction by LPS is mediated through cytokines. Normal (C3Heb/FeJ) and low cytokine-producing (C3H/HeJ) mice were given various doses of LPS, interleukin-1 (IL-1), interleukin-6 (IL-6), or tumor necrosis factor (TNF), and hepatic MT was determined 24 hr later by the Cd/hemoglobin assay. The low-cytokine-producing mice were much less responsive to the induction of MT by LPS (50 vs 150 micrograms MT/g liver after 1.0 mg LPS/kg, ip) than the normal mice, but were equally responsive to the induction of MT by IL-1 (0.03-1.0 microgram/mouse). IL-6 (0.5-5.0 micrograms/mouse), and TNF (0.005-0.5 microgram/mouse). All the cytokines produced a dose-dependent increase of hepatic MT levels in these two murine substrains (up to five- to sevenfold over controls). In conclusion, these data suggest that LPS induction of MT may be mediated through cytokines.
 ...
PMID:Endotoxin induction of hepatic metallothionein is mediated through cytokines. 206 24

The intervention of adrenaline in the immunoregulation was investigated through the modification of the anti-SRBC PFC response of mice after its i.p. administration (4 micrograms) at various intervals before SRBC antigen. When the interval was less than 24 h, adrenaline accelerated the immune kinetics. This modification was apparent on both direct and indirect PFC, as well as on naive and immune mice. However, mice treated from 2 days showed a suppression of the response. The adrenaline effect subsisted on the adoptive response of spleen cells drug-treated either in vivo or in vitro. The mitogenic response after in vitro PHA or LPS stimulation of spleen cells from adrenaline-treated mice indicated that the T-cells were the drug target. The physiological role of the adrenaline and immunological influences of acute stress are discussed in the paper.
 ...
PMID:Adrenaline influence on the immune response. I. Accelerating or suppressor effects according to the time of application. 645 57

Surfactant proteins A (SP-A) and D (SP-D) are "collectins": proteins with collagen-like region and lectin domain that bind carbohydrates in a calcium-dependent manner. Mannose-binding protein, a serum collectin, is an acute-phase protein. We hypothesized that SP-A and SP-D would respond to an acute stress, such as lung inflammation, in the same manner as does mannose-binding protein, with increased messenger ribonucleic acid (mRNA) and protein production. Rats received intratracheal lipopolysaccharide (LPS; 0.5 mg/kg) or vehicle and were killed 1, 6, 24, and 72 h later. Their lungs were lavaged and the lung tissue homogenized and analyzed for SP-A, SP-D, and phospholipids. Tissue levels of SP-A were increased by 6 h, peaked at 24 h, and were still elevated at 72 h in LPS-treated animals as compared with those given vehicle. SP-A and SP-D levels in lavage fluid were significantly elevated at 72 h. Message levels for SP-A and SP-D, but not SP-B, were significantly increased at 24 h. Lavage phospholipid levels first increased, then decreased in both the control and LPS-treated animals, and significantly less phospholipid was recovered in the lavage fluid of the LPS-treated animals than in that of controls at 72 h. Although other mechanisms, including altered surfactant metabolism, may be involved, these data are consistent with our hypothesis that SP-A and SP-D are upregulated by an acute inflammatory stress in a manner analogous to that of the structurally and functionally related serum acute-phase reactant, mannose-binding protein. We speculate that this upregulation may be a protective response for the lungs.
 ...
PMID:Surfactant proteins A and D increase in response to intratracheal lipopolysaccharide. 887 85

Acute stresses such as trauma or endotoxemia augment GLN demand and are associated with increased release of this amino acid from skeletal muscle and lung as well as increased expression of glutamine synthetase (GS, the principal enzyme of GLN synthesis) in these tissues. Muscle GLN release is also increased during chronic catabolic states which are associated with depletion of lean body mass, such as starvation or malignancy. We hypothesized that the expression of GS in response to an acute stress would be altered in tumor-bearing rats (TBR) experiencing severe cachexia and therefore a previously heightened GLN demand. Male Fischer 344 rats were implanted with methylcholanthrene-induced fibrosarcoma tumors or underwent sham operations and pair-feeding (sham) with TBR partners. When tumor burden reached approximately 15% of carcass weight, animals received injections of either Escherichia coli lipopolysaccharide (LPS, 1 mg/kg body wt) or saline vehicle. Rats were sacrificed 8 h after injection and lung and muscle tissue were analyzed for GS mRNA and protein via Northern and Western blot techniques, respectively. LPS injection caused an equivalent 4- to 6-fold increase in lung and muscle GS mRNA in both TBR and sham rats (P < 0.01). LPS did not produce a significant increase in GS protein level in muscle tissue of either group or in lung tissue of sham rats. In contrast, endotoxin did lead to a 3.5-fold increase in GS protein levels in lung tissue of TBRs (P < 0.05). This increase in lung GS protein may signify the importance of the lung in maintaining GLN homeostasis during chronic catabolic states where muscle mass is diminished.
 ...
PMID:Sepsis increases lung glutamine synthetase expression in the tumor-bearing host. 973 11

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.
 ...
PMID:Differential effects of psychological and immunological challenge on the hypothalamo-pituitary-adrenal axis function in adjuvant-induced arthritis. 1041 92

Adjuvant-induced arthritis (AA) in the rat is a T-cell mediated, chronic inflammatory stress in which circulating interleukin (IL)-6 levels are elevated. In addition, there are profound neuroendocrine changes associated with the development of hind-paw inflammation which have major implications for the ability of the rat to respond the to stress. Central injection of morphine is also able to increase circulating IL-6 concentration in control animals. In the present study we have determined the effects of a single injection of morphine into the lateral ventricle of control and AA animals on plasma corticosterone levels, on changes in plasma corticosterone and on IL-6 and IL-6 receptor mRNAs in the pituitary and adrenal gland. IL-6 and IL-6 receptor mRNAs were increased in the anterior pituitary of AA rats given moprhine compared with saline-treated AA rats. In the adrenal cortex, IL-6 mRNA was unaltered and IL-6 receptor mRNA was significantly decreased under these same conditions. AA rats were unable to mount corticosterone response to acute stress but were able to respond to acute stimulation with e.g. LPS. In the present study we found a sustained increase in plasma corticosterone in control animals which was still significantly elevated 2 hours following morphine injection, with a further significant increase in AA rats. These data suggest that alternative systems distinct from those activated in response to acute stress are activated by morphine in the AA animals. The similarity with the sustained increase in corticosterone following LPS injection suggest that either similar pathways are involved, or that central opiates may be involved in mediating HPA axis response to stress.
 ...
PMID:Central injection of morphine stimulates plasma corticosterone and interleukin (IL)-6 and IL-6 R mRNAs in the pituitary and adrenals in adjuvant-induced arthritis. 1050 33

Adjuvant-induced arthritis (AA) in the rat is a chronic inflammatory stress in which circulating corticosterone and interleukin (IL)-6 levels are elevated. In addition, there are profound neuroendocrine changes associated with the development of hind-paw inflammation which have major implications for the ability of the rat to respond to stress. Central injection of morphine is able to increase plasma corticosterone and circulating IL-6 concentration in control animals. In present study we have determined the effects of a single and repeated injection of morphine into the lateral ventricle of control and AA animals on plasma corticosterone, circulating IL-6 levels and course of hind-paw inflammation in AA rats. In the present study we found a sustained increase in plasma corticosterone both after single and repeated injection of morphine in control and AA rats and an increase of the level of circulating IL-6 in AA rats after repeated injection of morphine. These data suggest that alternative systems distinct from Athose activated in response to acute stress are activated by morphine in the AA animals. The similarity with the sustained increase in corticosterone following LPS injection suggest that central opiates may be involved in mediating HPA axis and cytokines response to inflammatory stress.
 ...
PMID:Central single and chronic administration of morphine stimulates corticosterone and interleukin (IL)-6 in adjuvant-induced arthritis. 1122 Apr 97

Using a combination of transcriptional profiling and Ingenuity Pathway Analysis (IPA, www.ingenuity.com) we investigated acute and chronic psychological stress induced alterations of hepatic gene expression of BALB/c mice. Already after a 2-h single stress session, up-regulation of several LPS and glucocorticoid-sensitive immune response genes and markers related to oxidative stress and apoptotic processes were observed. Support for the existence of oxidative stress was gained by measuring increased protein carbonylation, but no alterations of immune responsiveness or cell death were measured in mice after acute stress compared to the control group. When animals were repeatedly stressed during 4.5-days, we found reduced transcription of antigen presentation molecules, altered mRNA levels of immune cell signaling mediators and persisting high expression of apoptosis-related genes. These alterations were associated with a measurable immune suppression characterized by a reduced ability to clear experimental Salmonella typhimurium infection from the liver and a heightened hepatocyte apoptosis. Moreover, genes associated with anti-oxidative functions and regenerative processes were induced in the hepatic tissue of chronically stressed mice. These findings indicate that modulation of the immune response and of apoptosis-related genes is initiated already during a single acute stress exposure. However, immune suppression will only manifest in repeatedly stressed mice which additionally show induction of protective and liver regenerative genes to prevent further hepatocyte damage.
 ...
PMID:Altered hepatic mRNA expression of immune response and apoptosis-associated genes after acute and chronic psychological stress in mice. 1959 98

Little is known about CRF expression and regulation in the rat colon compared to the brain. We investigated CRF gene expression, cellular location, and regulation by endotoxin and corticosterone in the male rat colon at 6h after intraperitoneal (ip) injection. CRF mRNA level, detected by reverse transcription-polymerase chain reaction (RT-PCR) was 1.3-fold higher in the distal than proximal colon and 3.4-fold higher in the proximal colonic submucosa plus muscle layers than in mucosa. CRF immunoreactivity was located in the epithelia, lamina propria and crypts, and co-localized with tryptophan hydroxylase, a marker for enterochromaffin (EC) cells, and in enteric neurons. Lipopolysaccharide (LPS, 100 microg/kg, ip) increased defecation by 2.9-fold and upregulated CRF mRNA by 2.5-fold in the proximal and 1.1-fold in the distal colon while there was no change induced by corticosterone as monitored by quantitative PCR. LPS-induced increased CRF mRNA expression occurred in the submucosa plus muscle layers (1.5-fold) and the mucosa of proximal colon (0.9-fold). LPS increased significantly CRF immunoreactivity in the submucosal and myenteric plexuses of proximal and distal colon compared to saline groups. These results indicate that in rats, CRF is expressed in both proximal and distal colon and more prominently in enteric neurons of the submucosa plus muscle layers and subject to upregulation at the gene and protein levels by LPS through corticosteroid independent pathways. These data suggests that colonic CRF may be part of the local effector limb of the CRF(1) receptor mediated colonic alterations induced by acute stress.
 ...
PMID:Corticotropin releasing factor in the rat colon: expression, localization and upregulation by endotoxin. 1994 26

Co-species housing of mice and rats is common practice at most breeding facilities and research laboratories, neglecting the possible effects on the animals. We investigated physiological as well as behavioral stress-reactivity in mice and rats which were either derived from a co-species or species-separated housing condition at the breeding facilities. The animals were kept under the housing condition they were used to or assigned to the opposite one. Co-species housing had a significant impact on acute stress reactivity in mice and rats but only if they were used to this housing condition throughout their lives. Moreover, the stress-effects appeared to be long lasting. Assigning animals, derived from a species-separated housing condition, to co-species housing led to chronic stress in mice and affected experimental behavior of rats. Our findings led to the conclusion that co-species housing in mice and rats should be avoided, supporting the recommendations by the U.S. National Institutes of Health (NIH) and the Dutch Ministry of Health, Welfare and Sport (VWS). In order to support the interpretation, facilitate the reproducibility and comparability and subsequently the generalizability of experimental results, breeding facilities should at least provide detailed information about their housing conditions.
 ...
PMID:Co-species housing in mice and rats: effects on physiological and behavioral stress responsivity. 2007 42


1 2 Next >>