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PubMed1998

Identification of domains involved in superantigenicity of streptococcal pyrogenic exotoxin F (SpeF).

A series of 11 synthetic peptides of 30 amino acids, each with 10 amino acids overlap which spanned the entire sequence of streptococcal pyrogenic exotoxin F (SpeF), were employed in proliferation studies on human peripheral blood mononuclear cells (PBMCs). Regions 41-70, 141-170 and 181-210 were identified as important for SpeF-induced lymphocyte activation. Secondary structure predictions of these peptides showed similarities to regions in other superantigens known to be important for T cell mitogenicity. Furthermore, antisera specific to peptides covering amino acids 1-70 and 181-228 were able to inhibit SpeF-induced mitogenicity by 25% when pre-incubated with SpeF prior to PBMC activation.

Adjuvants, Immunologic↗
PubMed1987

Dexamethasone pre-treatment is antipyretic toward polyinosinic: polycytidylic acid, lipopolysaccharide and interleukin 1/endogenous pyrogen.

The effect of intravenously injected dexamethasone on the febrile response of rabbits to Polyinosinic: Polycytidylic acid (Poly I:C), lipopolysaccharide (LPS) and interleukin 1/endogenous pyrogen (IL1/E.P.) was studied. Dexamethasone (1 mg/kg) attenuated the febrile response to Poly I:C (5 micrograms/kg) but only if administered between 0.5 to 2 h before Poly I:C. If it was given after Poly I:C this resulted in a potentiation of the fever. Antagonism of the febrile response to Poly I:C by dexamethasone pre-treatment was dose-dependent and a maximal effect was observed with 3 mg/kg, a higher dose (6 mg/kg) resulted in a lesser effect on the Poly I:C fever. DEX injected alone (0.5-6 mg/kg) did not have any effect on body temperature. Fevers in response to LPS (50 ng/kg) and IL1/E.P. were also attenuated by dexamethasone. It is concluded that Poly I:C, LPS and IL1/E.P. induce fever by a common mechanism which is either directly or indirectly inhibited by dexamethasone.

Animals↗
PubMed1994

Major histocompatibility complex class II binding site for streptococcal pyrogenic (erythrogenic) toxin A.

Streptococcal pyrogenic exotoxin A (SPEA) is an important pathogenicity factor of group A streptococci. It is a member of the family of "superantigens" produced by Staphylococcus aureus and Streptococcus pyogenes and its T lymphocyte stimulating activity is involved into the pathogenesis of certain diseases caused by pyogenic streptococci. In this study we have produced and characterized recombinant SPEA molecules in Escherichia coli. These molecules are indistinguishable from natural SPEA in both T cell stimulatory and HLA class II binding activities. Human class II molecules are more efficient than mouse class II molecules in presenting SPEA to T cells. In binding tests to major histocompatibility complex class II-positive cells SPEA competes with staphylococcal enterotoxin B and A but not with toxic shock syndrome toxin-1.

Animals↗
PubMed1988

Cloning and characterization of the gene, speC, for pyrogenic exotoxin type C from Streptococcus pyogenes.

The structural gene of streptococcal pyrogenic exotoxin type C (SPE C) was cloned from the chromosome of Streptococcus pyogenes strain T18P into Escherichia coli using pBR328 as the vector plasmid. Subcloning enabled the localization of the gene (speC) to a 1.7 kb fragment. Partially purified E. coli-derived SPE C and purified streptococcal-derived SPE C, were shown to have the same molecular weight (23,800) and biological activities. A DNA probe, prepared from cloned speC, cross-hybridized with the structural genes of SPE A and SPE B indicating relatedness at the nucleotide level. The speC-derived probe also hybridized to a fragment of CS112 bacteriophage DNA containing the phage attachment site.

Bacterial Proteins↗
PubMed1992

Production of pyrogenic exotoxins in group A streptococci isolated from patients in Zagreb, Croatia.

The pyrogenic exotoxin profiles were determined of group A streptococci isolated from patients in Zagreb, Croatia in the period 1989-1990. A total of 12 strains were studied, five from patients with serious infections and seven from patients with uncomplicated infections. Serotypes M1 and M3 were found in seven (58%) patients. Seven strains produced exotoxin A and ten strains exotoxin B. The proportion of exotoxin A and B producing strains in patients with severe infections (3 patients respectively) was similar to that found in patients with uncomplicated infections (4 and 7 patients respectively).

Adult↗
PubMed1976

On the mechanism of pyrogenic action of ricin.

The incubation of rabbit white blood cells with ricin, the toxic protein of castor oil seeds, leads to the production of endogenous pyrogens. This induction can be inhibited by the antibiotics actinomycin D or cycloheximide. The results are discussed in terms of disturbed corticosteroid- and Mg2+-levels.

Animals↗
PubMed1979

Influence of antilymphocyte and antipolymorphonuclear sera on the pyrogenic effect of scarlet fever toxin.

The role played by lymphocytes in the pyretic response to scarlet fever toxin (ET) was studied in vivo using antilymphocyte serum (ALS). Two i.v. injections of ALS inhibited the pyretic response to a subsequent ET injection in rabbits. The course of endotoxin fever remained uninfluenced by ALS. Antipolymorphonuclear serum had no effect on the pyretic response to either of the toxins. Pretreatment with ALS also inhibited the skin reaction after i.d. injection of ET. These findings are further evidence a mediating role of lymphocytes in the biological effects of ET, among other things in the release of endogenous pyrogen.

Animals↗
PubMed2005

Release of TNF-alpha and IL-1beta from porcine brain endothelium corresponds to the pyrogenic potential of three marketed formulations of amphotericin.

BACKGROUND: Formulations of amphotericin include a deoxycholate suspension (d-Amph), an amphotericin-B lipid complex (Ablc), and a liposomal product (L-Amph). Fever is most frequent with d-Amph, intermediate with Ablc, and lowest with L-Amph. OBJECTIVE: To determine if the release of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1-beta (IL-1) from brain endothelium corresponds to the incidence of amphotericin fever. RESULTS: Release of TNF-alpha and IL-1beta after L-Amph treatment was similar to negative controls while after d-Amph treatment release was similar to lipopolysaccharide. Ablc treatment produced intermediate pyrogen release.NF-kappaB expression, a transcriptional regulator for TNF-alpha and IL-1beta genes, corresponded to this secretion pattern. TNF-alpha release was elevated 2 hours (p = 0.0021) after treatment while significant elevations in IL-1beta required 6 hours (p = 0.0009). CONCLUSION: Results from this in vitro study suggest that amphotericin fever may be directly mediated by brain endothelium. These experiments also suggest that amphotericin fever is initially mediated by TNF-alpha.

Amphotericin B↗
PubMed2000

Involvement of CRH in fever induced by a distinct pre-formed pyrogenic factor (PFPF).

OBJECTIVE: This study investigated the role of corticotrophin-releasing hormone (CRH) in mediating the fever induced by a novel pre-formed pyrogenic factor (PFPF), using a CRF antagonist in vivo and evaluating the capacity of PFPF to stimulate CRH release from the hypothalamus in vitro. MATERIALS AND METHODS: Male Wistar rats were used. The PFPF, induced following brief incubation of rat peritoneal macrophages with LPS and retained on 10 or 20 kDa MW cut-off membranes, was injected intracerebroventricularly. Fever was monitored using a rectal probe. Hypothalamus tissue was incubated with PFPF to establish its ability to induce CRH release. The CRH was measured by ELISA. RESULTS: PFPF induced a dose-dependent fever that was abolished by boiling or pronase treatment. Whereas both dexamethasone and indomethacin were effective in reducing interleukin- (IL) 1beta-induced fever, only dexamethasone abolished the fever induced by PFPF. The CRH antagonist, a-helical CRH9-41, abolished the fever induced by synthetic CRH, IL-8 and PFPF but not tumour necrosis factor-a (TNF-alpha). Like IL-1, PFPF was able to induce the release of CRH from rat hypothalamic tissue in vitro. CONCLUSIONS: These results suggest that the fever induced by PFPF depends on CRH release but not prostaglandin synthesis.

Animals↗
PubMed1994

Polyunsaturated fatty acids reduce pyrogen-induced tissue factor expression in human monocytes.

Endotoxin (LPS) and interleukin-1 beta (IL-1 beta) increased the expression of tissue factor, a membrane-anchored glycoprotein that initiates blood coagulation on the surface of cultured human umbilical vein endothelial cells (HUVEC) and human monocyte/macrophages. On monocyte/macrophages, oleic acid strongly inhibited LPS-induced tissue factor expression, a similar activity also being obtained with regard to the pyrogenic effects of IL-1 beta. Other polyunsaturated fatty acids such as linoleic or linolenic acid also reduced tissue factor expression whereas palmitic acid was ineffective. In contrast, these compounds showed no effect on LPS- or IL-1 beta-induced tissue factor expression in HUVEC when tested at the concentration of 10 microM. These data therefore suggest that the well-recognized antithrombotic and antiatherogenic effect of polyunsaturated fatty acids may in part be mediated through an inhibition of tissue factor expression in monocyte/macrophages.

Cell Line↗
PubMed1988

Comparative pyrogenic potency of endogenous prostanoids and of prostanoid-mimetics injected into the anterior hypothalamic/preoptic region of the cat.

In both pyrogen-induced fever and fever subsequent to acute hypothalamic trauma, pyrexia is believed to be mediated by cyclooxygenase products acting within the anterior hypothalamic/preoptic (AH/PO) region of the brain. The goal of the present study was to assess, through a potency analysis, the likely contributions of various prostanoids to pyrexia production. Prostanoids and prostanoid-mimetics were injected bilaterally into the AH/PO region of conscious, indomethacin pretreated cats, and partial dose-response curves for pyrexic activity were obtained. ED1 degrees doses (doses producing a 1 degree C fever) for PGE2, PGE1 and 6-keto-PGE1 (a metabolite of PGI2 and/or of the PGI2 hydrolysis product, 6-keto-PGF1 alpha) ranged between 2 and 15 pmol. PGF2 alpha and the stable PGI2-mimetics, iloprost and 6-beta-PGI1, required doses of 900-1100 pmol. PGD2 and 6-keto-PGF1 alpha had ED1 degrees doses of 2200-2400 pmol. PGI2, thromboxane (TX) B2 and the TXA2/PGH2-mimetics, SQ26655, 9,11-azo-PGH2 and U46619, were incapable of producing a 1 degrees C rise at the maximum dose of 30,000 pmol. The results offer no support for an involvement in fever of PGF2 alpha, PGD2, TXA2, TXB2, PGH2, PGI2 or 6-keto-PGF1 alpha. Only the 3 E-series prostaglandins were sufficiently potent to merit serious consideration as mediators of pyrexia. Of these, only PGE2 is known to be produced in abundance by cat brain; no information is available regarding PGE1 production, and our results with PGI2 and 6-keto-PGF1 alpha indicate that cat brain may not synthesize 6-keto-PGE1. The results thus suggest an important role for PGE2 in fever production in the cat and are compatible with an involvement of PGE1.

Animals↗
PubMed1988

Maturation of pyrogen-elicited fever in the kitten.

The febrile response to the endotoxin Salmonella typhosa was studied in developing kittens. We found that kittens younger than 30 days of age generated only a small rise in temperature in response to a standardized endotoxin challenge that consistently causes fever in adult cats. Some degree of febrile response was present at birth, but the dose of pyrogen necessary to elicit a fever was 10-15 times greater than that required in the adult. There was a gradual increase in both the magnitude and duration of fever as a function of age with the largest change occurring after 30 days of age. There was a direct relationship between the ability of the kitten to maintain its body temperature (Tbo) at the room ambient (Ta) and the magnitude of the elicited fever. However, increasing the Ta to thermoneutral (Ta = 30-32 degrees C) did not enhance the thermal response indicating that the failure to elicit the fever is not due to passive effects of Ta. These data suggest that the febrile response to an endotoxin develops over the first 6-7 weeks of the kitten's life and are discussed in relation to other physical variables of development.

Aging↗
PubMed1985

Purification of human interleukin 1 from human monocyte culture supernatants and identity of thymocyte comitogenic factor, fibroblast-proliferation factor, acute-phase protein-inducing factor, and endogenous pyrogen.

Human interleukin 1 (IL-1) in lipopolysaccharide and silica-stimulated human peripheral blood monocyte culture supernatants was purified to apparent homogeneity by sequential chromatography using DEAE-Sephacel, Sephacryl S-200, CM-high-performance liquid chromatography (HPLC), and hydroxyapatite-HPLC. Analysis by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) yielded only one band detectable by silver staining with an apparent molecular weight (MW) of 19,000 under nonreducing conditions. IL-1 activity was eluted from a single site from PAGE performed in the absence of SDS. About 4.4 micrograms of IL-1 was purified from 5.0 liters of culture supernatant of lipopolysaccharide- and silica-stimulated human peripheral blood monocytes, with 46.6% recovery of biological activity. The specific activity of the purified IL-1 was 4.3 X 10(7) U/mg protein. Amino acid composition analysis of the purified human IL-1 was similar to that previously described for murine IL-1. The purified IL-1 exhibited the biological activities previously attributed to IL-1, including thymocyte comitogenic activity, fibroblast proliferation activity, acute-phase protein (haptoglobin)-inducing activity, and endogenous pyrogen activity.

Acute-Phase Proteins↗
PubMed1993

IL-4 and IL-13 exhibit comparable abilities to reduce pyrogen-induced expression of procoagulant activity in endothelial cells and monocytes.

Endotoxin (LPS), interleukin-1 beta (IL-1) and tumor necrosis factor-alpha (TNF) increased the expression of tissue factor, a membrane-anchored glycoprotein that initiates blood coagulation on the surface of cultured bovine aortic endothelial cells (ABAE) and human monocytes. These compounds simultaneously reduced the amount of thrombomodulin on the endothelial cell surface, further contributing to the procoagulant activity of the endothelium or monocytes. On endothelial cells and monocytes, interleukin-4 (IL-4) and interleukin-13 (IL-13), a newly described lymphokine, both strongly inhibited LPS-induced tissue factor expression, a similar activity also being obtained with regard to the pyrogenic effects of IL-1 or TNF. When measured in parallel, IL-4 and IL-13 counteracted thrombomodulin down-regulation induced by LPS, IL-1 or TNF in endothelial cells. These results therefore show that both IL-4 and IL-13 protect the endothelial and the monocyte surface against inflammatory mediator-induced procoagulant changes.

Animals↗
PubMed1982

The inhibitory effect of polymyxin B on endotoxin-induced endogenous pyrogen production.

The effect of polymyxin B (PMB) on the endogenous pyrogen (EP)-induced property of lipopolysaccharide (LPS) in vitro was examined. PMB inhibited LPS when added to leukocyte suspension 5 min before or up to 30 min after the addition of LPS. The inhibitory effect was dose-related and appeared to be specific for LPS (including naturally occurring endotoxin). EP production in response to a different stimulus (staphylococci) was not prevented even when LPS-PMB complexes were presumably present. These data suggest that when experimental agents are found to stimulate the production of EP or lymphocyte activating factors (LAF, interleukin-1) in vitro, or when apparently spontaneous production of EP or LAF is seen, incubation with PMB may be a useful technique to exclude th effects of endotoxin contamination - especially when negative results have been obtained in the limulus gelation test.

Animals↗
PubMed1990

A mutant protein of human interleukin-1 beta with immunostimulatory but not pyrogenic potency.

Interleukin-1 (IL-1) mediates a variety of immune and inflammatory responses. In order to understand the mechanisms involved in multiple biological functions, it is important to define the active sites of IL-1. Using the technique for site-specific mutagenesis, we tested whether the arginine residue at the 4th position in human IL-1 beta is essential for multiple biological activities. In our experiments, the fourth position is replaced by a non-basic amino acid--either glycine or aspartic acid. The resulting mutant protein shows both immunostimulatory activity and the ability to induce hematopoietic growth factors similar to native IL-1 beta, but has a markedly reduced pyrogenic potency. Therefore, the mutant protein of IL-1 beta may represent a good candidate for use in vivo as an adjuvant for poor immunogenic vaccines.

Adjuvants, Immunologic↗
PubMed1993

Chelerythrine, a selective protein kinase C inhibitor, counteracts pyrogen-induced expression of tissue factor without effect on thrombomodulin down-regulation in endothelial cells.

Endotoxin, interleukin 1 beta (IL-1 beta) and tumor necrosis factor alpha (TNF-alpha) dose-dependently increased the expression of tissue factor and at the same time induced thrombomodulin down-regulation on the surface of cultured bovine aortic endothelial cells. Chelerythrine, a selective protein kinase C inhibitor, strongly reduced endotoxin-, IL1 beta- and TNF alpha-induced tissue factor expression but remained without effect with regard to thrombomodulin down-regulation measured in parallel. On the contrary, staurosporine, a highly potent, non-selective PKC inhibitor, simultaneously abolished tissue factor expression and thrombomodulin down-regulation induced by endotoxin, IL1 beta and TNF alpha. These results show that protein kinase C is deeply involved in the process leading to pyrogen-induced tissue factor expression and suggest that thrombomodulin down-regulation is regulated by a different pathway.

Alkaloids↗
PubMed1991

Preliminary assessment of removal of pyrogenic lipopolysaccharides with colloidal zirconia adsorbents.

Preliminary evaluation of bare or polymer-coated colloidal monoclinic zirconia of nominal particle size 100 nm indicated that it is an effective adsorbent for pyrogenic lipopolysaccharides (LPS) as measured by chemical and Limulus amebocyte lysate (LAL) assays. Zirconia at 50 micrograms ml-1 adsorbed 99.95% of added E. coli O128 LPS. Residual LPS levels below 0.1 ng ml-1 were easily attained. Colloidal zirconia was able to remove LPS from solution in the presence of bovine albumin (BSA). Some LPS contaminating BSA lacked affinity for zirconia. Preadsorption of phosphate onto bare zirconia blocked LPS adsorption. However, phosphated-oligomeric glycidyl (epoxy) pentaerythritol-coated colloidal zirconia could be derivatized with imidazole-containing ligands to produce an LPS-binding surface. Preliminary results of adsorption of LPS by the coated particles indicated a reduced level of LPS binding compared to bare zirconia, probably because the particles aggregated during the derivatization process, reducing the effective surface available for LPS adsorption.

Adsorption↗