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PubMed1999

Marked instability of the sigma(32) heat shock transcription factor at high temperature. Implications for heat shock regulation.

The heat shock response in Escherichia coli depends on a transient increase in the intracellular level of sigma(32) that results from both increased synthesis and transient stabilization of normally unstable sigma(32). Although the membrane-bound ATP-dependent protease FtsH (HflB) plays an important role in degradation of sigma(32), our previous results suggested that several cytosolic ATP-dependent proteases including HslVU (ClpQY) are also involved in sigma(32) degradation (Kanemori, M., Nishihara, K., Yanagi, H., and Yura, T. (1997) J. Bacteriol. 179, 7219-7225). We now report on the ATP-dependent proteolysis of sigma(32) by purified HslVU protease and its unusual dependence on high temperature: sigma(32) was rapidly degraded at 44 degrees C, but with much slower rates ( approximately 15-fold) at 35 degrees C. FtsH-dependent degradation of sigma(32) also gave similar results. In agreement with these results in vitro, the turnover of sigma(32) in normally growing cells at high temperature (42 degrees C) was much faster than at low temperature (30 degrees C). Taken together with other evidence, these results suggest that the sigma(32) level during normal growth is primarily determined by the stability (susceptibility to proteases) and synthesis rate of sigma(32) set by ambient temperature, whereas fine adjustment such as transient stabilization of sigma(32) observed upon heat shock is brought about through monitoring changes in the cellular state of protein folding.

ATP-Dependent Proteases↗
PubMed2000

Canonical heat shock element in the alpha B-crystallin gene shows tissue-specific and developmentally controlled interactions with heat shock factor.

Oligomerization of the heat shock factor (HSF) and its interaction with the heat shock element (HSE) are the hallmark of active transcriptional response to tangible physical or chemical stress. It is unknown if these interactions are subject to control and modulation by developmental cues and thus have tissue or stage specificity. By using promoter sequences containing a canonical HSE from the alphaB-crystallin gene, we demonstrate a tissue-specific transition from monomeric (in fetal and early neonatal stages that lack oligomeric HSF.HSE complexes) to oligomeric HSF-HSE interactions by postnatal day 10-21 in the ocular lens. Developmental control of these interactions is further demonstrated by induction of oligomeric HSF.HSE complexes in neonatal extracts by in vitro manipulations, interestingly, only in the lens and not in the brain, heart, or liver extracts. The exclusive presence of oligomeric HSF.HSE complexes in the postnatal/adult lens corresponds to known highly increased number of alphaB-crystallin transcripts in this tissue.

Animals↗
PubMed2005

Preheating accelerates mitogen-activated protein (MAP) kinase inactivation post-heat shock via a heat shock protein 70-mediated increase in phosphorylated MAP kinase phosphatase-1.

Heat shock (HS) activates mitogen-activated protein (MAP) kinases. Although prior exposure to nonlethal HS makes cells refractory to the lethal effect of a subsequent HS, it is unclear whether this also occurs in MAP kinase activation. This study was undertaken to evaluate the effect of a heat pretreatment on MAP kinase activation by a subsequent HS and to elucidate its possible mechanism. Preheating did not make BEAS-2B cells refractory to extracellular signal-regulated protein kinase (ERK) and c-Jun N-terminal kinase (JNK) activation by a second HS but accelerated their inactivation after HS. The rapid inactivation of ERK and JNK was dependent on de novo protein synthesis and associated with the up-regulation of heat shock protein 70 (HSP70). Moreover, the inhibition of phosphatase activity reversed this rapid inactivation. MAP kinase phosphatase-1 (MKP-1) expression was increased by HS, and the presence of its phosphorylated form (p-MKP-1) correlated with the observed rapid ERK and JNK inactivation. Blocking induction of p-MKP-1 with antisense MKP-1 oligonucleotides suppressed the rapid inactivation of ERK and JNK in preheated cells. HSP70 overexpression caused the early phosphorylation of MKP-1. Moreover, MKP-1 phosphorylation and the rapid inactivation of ERK were inhibited by blocking HSP70 induction in preheated cells. In addition, MKP-1 was insolubilized by HS, and HSP70 associated physically with MKP-1, suggesting that a chaperone effect of HSP70 might have caused the early phosphorylation of MKP-1. These results indicate that preheating accelerated MAP kinase inactivation after a second HS and that this is related to a HSP70-mediated increase in p-MKP-1.

Adenoviridae↗
PubMed1983

Is the major Drosophila heat shock protein present in cells that have not been heat shocked?

When eukaryotic cells are exposed to elevated temperatures they respond by vigorously synthesizing a small group of proteins called the heat shock proteins. An essential element in defining the role of these proteins is determining whether they are unique to a stressed state or are also found in healthy, rapidly growing cells at normal temperatures. To date, there have been conflicting reports concerning the major heat-induced protein of Drosophila cells, HSP 70. We report the development of monoclonal antibodies specific for this protein. These antibodies were used to assay HSP 70 in cells incubated under different culture conditions. The protein was detectable in cells maintained at normal temperatures, but only when immunological techniques were pushed to the limits of their sensitivity. To test for the possibility that these cells contain a reservoir of protein in a cryptic antigenic state (i.e., waiting posttranslational modification for use at high temperature), we treated cells with cycloheximide or actinomycin D immediately before heat shock. HSP 70 was not detected in these cells. Finally, we tested for the presence of a reservoir of inactive messages by using a high stringency hybridization of 32P-labeled cloned gene sequences to electrophoretically separated RNAs. Although HSP 70 mRNA was detectable in rapidly growing cells, it was present at less than 1/1,000th the level achieved after induction.

Animals↗
PubMed1999

Randomized, placebo-controlled trial of HA-1A, a human monoclonal antibody to endotoxin, in children with meningococcal septic shock. European Pediatric Meningococcal Septic Shock Trial Study Group.

Meningococcal septic shock has a rapid onset and characteristic skin hemorrhages that allow bedside diagnosis. Initial plasma endotoxin levels are high and correlate closely with clinical outcome. In a double-blind, randomized, placebo-controlled trial (planned, n = 270; actual, n = 269), we compared the effectiveness of HA-1A (6 mg/kg of body weight iv; maximum, 100 mg), a human monoclonal antibody to endotoxin, and placebo in reducing the 28-day all-cause mortality rate among children with a presumptive clinical diagnosis of meningococcal septic shock. Treatment groups were well balanced for baseline characteristics and prespecified prognostic variables. In this trial no significant benefit of HA-1A could be demonstrated. The 28-day mortality rates in the intention-to-treat analysis were as follows: placebo, 28%; HA-1A, 18%; reduction in mortality, 33% (P = .11, per Fisher's exact test, two-tailed; odds ratio = 0.59; 95% confidence interval for the difference, 0.31-1.05). All patients tolerated HA-1A well, and no antibodies to HA-1A were detected.

Antibodies, Monoclonal↗
PubMedDate not supplied

Ecology of toxic shock syndrome: amplification of toxic shock syndrome toxin 1 by materials of medical interest.

Historically, the literature suggests that staphylococcal exoproteins, including enterotoxins, are stimulated by various physicochemical ecologic factors, many of which have been shown to stimulate production of toxic shock syndrome toxin 1 (TSST-1). The propensity of different fibers and other substances to amplify TSST-1 production in toxic shock syndrome-associated strains of Staphylococcus aureus, as well as a comparative analysis of the underlying mechanisms of TSST-1 production, are reported. Two hundred twenty intravaginal devices or other products and materials and 60 experimental controls were examined for their propensity to induce TSST-1 production. Certain materials are superior to unaltered cotton in providing a more absorbent fiber--nutrients are efficiently drawn in, concentrating protein between fibers, and thereby creating an ideal physicochemical environment for the amplification of TSST-1 and other toxins. The greatest stimulation of TSST-1 was observed with (in decreasing order): polyester and carboxymethyl cellulose, polyacrylates, viscose rayon, gelatin foam, polyurethane, and cotton. No toxin was found with nasal tampons (polymer of polyvinyl acetal) or with vaginal cups (an elastomeric polymer). Results are discussed in terms of specific ecologic parameters from historical as well as recent perspectives.

Bacterial Toxins↗
PubMedDate not supplied

Effects of drugs on the pyrogenicity of toxic shock syndrome toxin 1 and its capacity to enhance susceptibility to the lethal effects of endotoxic shock in rabbits.

The effects of various kinds of drugs on the pyrogenicity of toxic shock syndrome toxin 1 (TSST-1) and its capacity to enhance the lethal effects of endotoxin in rabbits were studied. Antipyretic agents--including aspirin, aminopyrine, and indomethacin--that were given immediately or 2 hours after injection of TSST-1 decreased the febrile response to TSST-1 but did not inhibit the enhancement of lethality. Cyclosporine, which was given 2 hours after injection of TSST-1, suppressed the fever but did not inhibit the lethal effects. Methylprednisolone given immediately or 2 hours after TSST-1 injection did not decrease the fever but inhibited the lethal effect. Of the agents phentolamine, dopamine, and chlorpromazine, which are reported to suppress endotoxic shock experimentally, only chlorpromazine decreased the fever, and none inhibited the lethal effects.

Animals↗
PubMed1985

Development of serum antibody to toxic shock toxin among individuals with toxic shock syndrome in Wisconsin.

The presence of Staphylococcus aureus producing toxic shock toxin (TST) and the absence of antibody to TST (anti-TST) in acute-phase sera are markers for toxic shock syndrome (TSS). We used radioimmunoassay methods to examine 133 acute-phase and 277 convalescent-phase serum specimens from 181 patients with TSS for anti-TST. Among confirmed menstrual cases, nine (9.5%) of 95 patients had demonstrable anti-TST in acute-phase sera obtained during the first seven days of illness; patients with probable or non-menstrual TSS had a higher prevalence of anti-TST in acute-phase sera. Five (33.3%) of 15 individuals with confirmed menstrual TSS developed anti-TST as early as seven to nine days after TSS onset; 32 (62.7%) of 51 patients had demonstrable anti-TST in sera obtained more than one year after their episode of TSS. This study demonstrates a gradual rate and low magnitude of development of anti-TST after TSS and supports the diagnostic usefulness of measuring anti-TST levels in sera from patients suspected of having TSS.

Acute Disease↗
PubMedDate not supplied

Shock thyroid: A new manifestation of the hypovolemic shock complex in trauma patients.

The authors describe a new computed tomography finding associated with significant thoracoabdominal trauma: thyroidal and perithyroidal edema and fluid without evidence for direct thyroid injury. It does not seem to be related to direct or indirect thyroid injury but is rather a secondary finding related to the hypovolemic shock complex. The physiology of this phenomenon is unknown, but it is likely to be an additional component to the imaging findings of the hypovolemic shock complex. This finding should be recognized so as to avoid confusion with thyroid or vascular injury or other incidental etiology.

Accidents, Traffic↗
PubMed1984

Expression of a Drosophila heat shock protein in mammalian cells: transient association with nucleoli after heat shock.

We transformed mouse L cells with a cloned Drosophila hsp70 gene and obtained cells with either heat-inducible or constitutively expressed copies of the gene. The distribution of hsp70 in these cells was examined by indirect immunofluorescence with monoclonal antibodies specific to the Drosophila protein. In constitutive cells, hsp70 was present in both cytoplasm and nucleus. After heat shock, the nuclear hsp70 was transiently concentrated in nucleoli, from which it had previously been excluded; the cytoplasmic hsp70 moved to a perinuclear location, a result consistent with it being associated with intermediate filaments of the cytoskeleton. The nucleolar migration took several hours and was partly inhibited by actinomycin D, but was independent of protein synthesis; it may reflect binding to newly-synthesized rRNA. Drosophila hsp70 was also expressed from replicating plasmids in monkey COS cells, and was found to be concentrated in nuclei even at low temperature. Migration to nucleoli occurred after heat shock. These results indicate that a single protein can have multiple interactions with cellular components, and form the basis for future studies of these interactions by in vitro mutagenesis and expression of the hsp70 gene.

Animals↗
PubMed1992

Heat-shock response in cultured chick embryo chondrocytes. Osteonectin is a secreted heat-shock protein.

We investigated the induction of specific protein expression by heat shock in dedifferentiated and hypertrophic chick embryo chondrocytes in a culture system that allows 'in vitro' differentiation of cartilage cells [Castagnola, P., Moro, G., Descalzi-Cancedda, F. and Cancedda, R. (1986) J. Cell. Biol. 102, 2310-2317]. As control, we used cultures of embryonic fibroblasts from the whole body and from the skin. In the cell lysates of all cultures we identified four major heat-shock proteins (HSP), with a molecular size corresponding to HSP families previously described (HSP 90, HSP 70, HSP 47 and HSP 26). Some of these proteins were constantly induced when the temperature was raised, others were expressed in a more variable manner. Differences also existed in the relative amount of the HSP synthesized by the four cultures. When we specifically investigated HSP species released into the culture medium, we observed a 43-45 kDa protein constantly expressed and secreted in large amount by the cells. On the basis of its biochemical characteristic and its precipitation by specific antibodies, this protein has been identified as osteonectin (SPARC, BM-40).

Animals↗
PubMed1984

Association of high levels of serum antibody to staphylococcal toxic shock antigen with nasal carriage of toxic shock antigen-producing strains of Staphylococcus aureus.

Forty-four asymptomatic male subjects were examined for their nasal carriage of strains of Staphylococcus aureus capable of producing staphylococcal toxic shock antigen (TSA), an exotoxin implicated in the pathogenesis of toxic shock syndrome. In addition, the levels of antibody to TSA in sera from these subjects were determined by an enzyme-linked immunosorbent assay. S. aureus was isolated from the anterior nares of 23 subjects. Of those 23 isolates of S. aureus, 9 were found to produce TSA. All individuals carrying strains of S. aureus capable of producing TSA had high to moderate levels of antibody to TSA. In contrast, those individuals carrying strains not producing TSA had levels of antibody to TSA ranging from high to nondetectable. A second examination of nasal samples from 42 of these subjects revealed that 86% of those carrying S. aureus initially still carried S. aureus after a period of 3 months; all subjects found to carry TSA-producing strains initially and that were examined a second time yielded TSA-producing strains once again.

Adult↗
PubMed1987

A rabbit model of toxic shock syndrome that uses a constant, subcutaneous infusion of toxic shock syndrome toxin 1.

We have developed a rabbit model of toxic shock syndrome that uses a subcutaneous infusion pump to administer toxic shock syndrome toxin 1 (TSST-1). A dose of 150 micrograms, infused at a constant rate over a period of 7 days, resulted in a characteristic illness highlighted by fever, conjunctival hyperemia, cachexia, and lethargy. The illness was uniformly fatal, with a mean interval until death of 3.2 +/- 0.4 days. Serial determinations of serum chemistries confirmed the multisystem nature of this illness. Rabbits developed profound hypocalcemia, with levels falling from 15.5 +/- 0.2 to 7.6 +/- 0.4 mg/dl under the influence of TSST-1. Blood urea nitrogen and creatinine rose dramatically, in the setting of oliguria or anuria. Serum glutamicpyruvic transaminase was the most reliable indicator of hepatic dysfunction, with the mean rising from 48 U/liter before administration of TSST-1 to 546 U/liter among rabbits surviving 2 days of the infusion. Creatine phosphokinase also rose dramatically in 10 of 16 rabbits. Rabbits demonstrated relative neutrophilia and lymphopenia as well as an increase in the partial thromboplastin time. Histopathologic examination demonstrated disease of multiple organs, particularly the liver, spleen, and lymph nodes, all of which demonstrated inflammation, thrombosis, hemorrhage, and erythrophagocytosis. The concurrent administration of prednisolone with TSST-1 prevented death in four of four rabbits and greatly lessened the morbidity. Rabbits were not protected from morbidity or mortality by the concurrent administration of polymyxin B. We believe that a constant, subcutaneous infusion of TSST-1 in rabbits provides a reproducible model for studying the pathogenesis of TSS.

Adrenal Cortex Hormones↗
PubMed2006

Expression of heat shock protein 27 in human atherosclerotic plaques and increased plasma level of heat shock protein 27 in patients with acute coronary syndrome.

BACKGROUND: We intended to identify proteins that are differentially expressed in human atherosclerotic plaques. METHODS AND RESULTS: Comparative 2-dimensional electrophoretic analysis on carotid atherosclerotic endarterectomy specimens (n = 10) revealed that heat shock protein 27 (Hsp27) expression was significantly increased in the nearby normal-appearing area compared with the plaque core area from the same vessel specimen, which was further confirmed by Western blot analysis. The Hsp27 expression in the adjacent normal-appearing vessel areas was much higher than that in nonatherosclerotic reference arteries. The phosphorylation of Hsp27 showed a gradation in the degree of phosphorylation: greatest in the reference arteries, intermediate in the adjacent normal-appearing area, and lowest in plaque core area. Immunohistochemical analysis showed that the phosphorylation of Hsp27 of smooth muscle cells in the carotid endarterectomy specimens was decreased compared with that in the reference artery specimen. The mean plasma level of Hsp27 was significantly higher in patients with acute coronary syndrome (ACS) (n = 27; 106.1 +/- 74.1 ng/mL) than in the normal reference subjects (n = 29; 45.8 +/- 29.5 ng/mL; P < 0.005). The plasma levels of Hsp27 were significantly correlated with those of heat shock protein 70 (Hsp70) (r = 0.422, P < 0.0005), with adjustment for ACS/reference status. CONCLUSIONS: In the atherosclerotic lesion, Hsp27 expression is increased in the normal-appearing vessel adjacent to atherosclerotic plaque, whereas levels in the plaque itself are significantly decreased. Both plaque and adjacent artery show decreased Hsp27 phosphorylation compared with reference vessel. In ACS, plasma Hsp27 and Hsp70 are increased, and levels of Hsp27 correlate with Hsp70, C-reactive protein, and CD40L levels.

Adult↗
PubMed1999

Staphylococcus aureus isogenic mutant, deficient in toxic shock syndrome toxin-1 but not staphylococcal enterotoxin A production, exhibits attenuated virulence in a tampon-associated vaginal infection model of toxic shock syndrome.

Since menstrual toxic shock syndrome (MTSS) is associated with a predominant clone of Staphylococcus aureus which produces both toxic shock syndrome toxin-1 (TSST-1) and staphylococcal enterotoxin A (SEA), we sought to clarify the role of TSST-1 in a tampon-associated vaginal infection model in New Zealand White (NZW) rabbits, using isogenic tst+/sea+ S. aureus mutants in which tst was inactivated by allelic replacement. Rabbits infected with the tst-/sea+ strain became ill within 3 days, with fever, weight loss, conjunctival hyperemia, and lethargy. Mortality was significantly higher with the tst+/sea+ strain compared to its tst-/sea+ isogenic derivative (4/13 vs. 0/14; p < 0.05, Fisher's exact test, 2-tailed). Mean fever index was higher (p < 0.005; t test, 2-tailed) and weight loss more sustained among survivors in the tst+/sea+ group. Furthermore, culture filtrates from the tst+/sea+ strain induced a significantly greater response in mitogenesis and TNF alpha secretion from rabbit splenocytes in vitro compared to the tst-/sea+ isogenic derivative. Thus, regardless of the role of SEA, TSST-1 significantly contributed to both morbidity and mortality in this tampon-associated vaginal infection model in NZW rabbits. This is the first demonstration of the potential role of TSST-1 and SEA in the pathogenesis of MTSS with a MTSS-associated clinical S. aureus strain in a relevant animal model.

Animals↗
PubMed1992

[Use of pneumatic anti-shock equipment (MAST = military anti-shock trousers) in prehospital emergency treatment. A review].

Employment of pneumatic anti-shock (MAST) equipment is a therapeutic possibility in some countries for hypovolaemic and shocked patients. This treatment may be associated with particularly serious side effects and no documentation is available to prove that MAST is beneficial for the patients. The only meticulous clinically controlled investigation concludes that MAST is without effect in city regions with well-trained paramedical or medical staff and employment of MAST can thus not be recommended. The effect of MAST outside urban regions is unknown and should be assessed by means of a clinically controlled investigation.

Denmark↗
PubMed1989

Correlation between the induction of heat shock protein 70 and enhanced viral reactivation in mammalian cells treated with ultraviolet light and heat shock.

Enhanced viral reactivation (EVR) is considered to be one manifestation of an inducible response to DNA damage in mammalian cells analogous to the SOS response in Escherichia coli. EVR is characterized by the increased survival of ultraviolet (UV)-irradiated virus in cells which have been pretreated with DNA-damaging agents or by another type of cellular stress, heat shock (HS). In this study, we have analyzed the induction of nuclear proteins from Vero cells treated with either UV or HS, with the goal of identifying the protein(s) which mediate the EVR response. Results of 2-dimensional protein gel electrophoresis and fluorographic analysis of [35S]methionine-labeled nuclear proteins showed that UV-irradiation caused the increased synthesis of five proteins at 4-9 h after treatment. At 19-24 h, one of these proteins was still being synthesized at a higher level in UV-irradiated cells, and there were nine additional proteins whose syntheses were enhanced over control levels. In contrast, HS induced only one Mr 72,000 nuclear protein whose synthesis was maximal during the 4-9-h labeling period and corresponded to one of the proteins induced by UV at 19-24 h. Subsequent Western and Northern blot analyses have confirmed that this protein is a member of the heat shock protein (hsp) 70 family. Elevated nuclear levels of this protein correlated temporally with the maximum EVR response induced by each treatment (4 h after HS and 24 h after UV). Since the kinetics of EVR is different following UV and HS and parallels the difference in the induction of nuclear levels of hsp70 following each treatment, the results suggest that hsp70 may be involved in mediating the EVR response. In addition, this protein may also play a role in the recovery of DNA synthesis in UV-irradiated cells.

Blotting, Northern↗