PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Pyrogens”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 379 records · Page 21Linked to original sources
PubMed1968

Host-parasite relationships among group A streptococci. IV. Suppression of antibody response by streptococcal pyrogenic exotoxin.

In rabbits, purified streptococcal pyrogenic exotoxin, at 0.002 of the ld(50) dose, suppressed the antibody response to injected sheep erythrocytes. The antibody suppressed was determined by density gradient ultracentrifugal analysis to be of the 19S class. Background serum antibody (50% hemolytic units), as determined photometrically, correlated well with background antibody-forming spleen cells, as determined by the hemolytic-plaque technique. The exotoxin induced neither positive nor negative changes in background antibody levels, but suppressed the early secondary response to injected antigen. A comparison and control experiment showed that purified gram-negative bacterial endotoxin at identical protocol did not induce antibody suppression, but did induce the well-known adjuvant effect. Because streptococcal pyrogenic exotoxin is known to inhibit the phagocytic function of the reticuloendothelial system (RES), these data strongly support the concept that antigen is processed by cells of the RES before it evokes a secondary immune response. The results also demonstrated that streptococcal pyrogenic exotoxin may play a unique role in lowering the acquired defense of the host against infection. If the anamnestic immune response of the host is temporarily suppressed, then the host-parasite balance would be upset in favor of the parasite.

Animals↗
PubMed1976

Changes in body temperature produced by prostaglandins and pyrogens in the chicken.

Bacterial pyrogen from S. abortus equi (SAE) was injected into the wing veins of chickens. Following injection of 0.05-0.5 mug SAE, body temperatures did not change significantly, whereas 2.0 or 10 mug of pyrogen caused falls in body temperature of 0.56 +/- 0.10degrees C and 1.1 +/- 0.21degrees C (mean +/- SE, n=5). The temperature falls were accompanied by a flushing of the comb and an increase in respiratory rate and were not antagonized by 1.0 g of acetylsalicylic acid (ASA) given orally. The injection of SAE (0.1 mug in 1 mul) into the anterior hypothalamus produced fevers averaging 1.24 +/- 0.07 degrees C (n=9) which were antagonized by oral ASA. Injections of SAE at other brainstem loci produced no temperatur changes. Seven chickens were also injected with 0.1 mug PGE in 1.0 mul into the anterior hypothalamus, and they developed fevers averaging 0.90 +/- 0.16 degrees C. The results support the concept that prostaglandins may be involved in fever in chickens but suggest that the action of pyrogen injected intravenously may be different from that following its injection directly into the hypothalamus.

Animals↗
PubMed1984

Sleep-promoting effects of endogenous pyrogen (interleukin-1).

When infused into the lateral cerebral ventricles of rabbits, human endogenous pyrogen (EP) preparations induced dose-dependent increases in slow-wave sleep concomitant with increasing body temperature. Heating EP to 70 degrees C destroyed its sleep-promoting and pyrogenic activity. Anisomycin (an antipyretic) prevented EP from increasing body temperature without affecting its sleep-promoting activity. Intravenous injection of EP induced fever and transient increases in slow-wave sleep but failed to induce prolonged increases in slow-wave sleep. We conclude that the somnogenic activity of EP is not secondary to its pyrogenic activity.

Animals↗
PubMed1998

A cluster of bloodstream infections and pyrogenic reactions among hemodialysis patients traced to dialysis machine waste-handling option units.

From June 17 through November 15, 1995, ten episodes of Enterobacter cloacae bloodstream infection and three pyrogenic reactions occurred in patients at a hospital-based hemodialysis center. In a case-control study limited to events occurring during October 1-31, 1995, seven dialysis sessions resulting in E. cloacae bacteremia or pyrogenic reaction without bacteremia were compared with 241 randomly selected control sessions. Dialysis machines were examined, dialysis fluid and equipment were cultured, and E. cloacae isolates were genotyped by pulsed-field gel electrophoresis. Each dialysis machine had a waste-handling option (WHO) through which dialyzer-priming fluid was discarded before each dialysis session; in 7 of 11 machines, one-way check valves designed to prevent backflow from the WHO into patient bloodlines were dysfunctional. In the case-control study, case sessions were more frequent when machines with >/=1 dysfunctional check valves were used. E. cloacae with identical pulsed-field gel electrophoresis patterns were isolated from case patients, dialysis fluid, station drains, and WHO units. Our investigation shows that bloodstream infections and pyrogenic reactions were caused by backflow from contaminated dialysis machine WHO units into patient bloodlines. The outbreak was terminated when WHO use was discontinued, check valves were replaced, and dialysis machine disinfection was enhanced.

Adult↗
PubMed1998

[A new test for the detection of pyrogens in pharmaceutical products. Examinations for the validation of the human whole blood assay]

The human whole blood assay utilises the natural fever response to detect pyrogens by determination of the release of IL-1beta. In order to replace the official method, the rabbit pyrogen test, a validation of the whole blood assay is necessary. A comparison of the results obtained from many blood samples has revealed the following: 1) Blood not stimulated by LPS does not produce IL-1beta. 2) Stimulation by LPS induces a concentration-dependent release of IL-1( beginning at a concentration of between 2-5 pg/mL LPS. 3) The amount of IL-1beta released varies greatly between samples obtained from different individuals. 4) Storing blood samples results in a right shifted LPS/IL-1beta curve with a steeper gradient and higher maximum value of IL-1beta. In this paper we suggest an experimental method for the determination of pyrogens based on the established semi-quantitative LAL gelation method as detailed in the European Pharmacopeia. Using this methodology, we were able to show that the amount of endotoxin in a number of different infusion solutions was below the LAL-endotoxin limit concentration. LPS was quantitatively determined from spiked samples.

Journal Article↗
PubMed1992

A moderate dose of cycloheximide does not prevent the febrile response to endotoxin but interfere with induction of pyrogenic tolerance in rabbit.

The purpose of the present study was to examine the effect of cycloheximide (Cx)--inhibitor of protein synthesis, on the development of pyrogenic tolerance to LPS. It has been observed that Cx at a dose of 1 mg/kg given intravenously 1 h prior to LPS did not prevent fever response, however it modified the induction of pyrogenic tolerance. It was manifested in existence of the second phase of fever after the following administrations of LPS into rabbits pretreated with Cx. In control group of rabbits the induction of pyrogenic tolerance was accompanied with decaying of the second peak of fever visible as early as the second dose of LPS.

Animals↗
PubMed1992

Fever in young lambs: hypoxemia alters the febrile response to a small dose of bacterial pyrogen.

Experiments were done on eight young lambs to investigate the effects of hypoxemia on the body temperature, metabolic and cardiovascular responses to intravenous administration of a small dose of bacterial pyrogen (0.3 micrograms lipopolysaccharide extracted from Salmonella Abortus Equi; SAE). Each lamb was anaesthetized with halothane and prepared for sleep staging and measurements of cardiac output, arterial and mixed-venous haemoglobin oxygen saturations, body-core and ear-skin temperatures. Three experiments were done on each lamb, the first being done no sooner than three days after surgery. The first experiment consisted of establishing the thermal neutral environment during normoxemia (ie, environmental temperature at which total body oxygen consumption was minimal while body temperature was maintained) for each lamb. The second and third experiments were done at the lamb's thermoneutral environment as determined on day 1. One experiment was done during normoxemia (ie, control condition, SaO2 approximately 90%) and one experiment was done during hypoxemia (ie, experimental condition, SaO2 approximately 50%). Measurements were made during a control period and during one-minute experimental periods at 10 minute intervals for 120 minutes following administration of 0.3 micrograms of bacterial pyrogen in sterile saline. Administration of SAE produced a short-lived fever of about 0.8 degrees C in the normoxemic lambs, whereas no change in body-core temperature was observed in the hypoxemic lambs. During normoxemia, the increase in body-core temperature was preceded by peripheral vasoconstriction, the onset of shivering, and a surge in total body oxygen consumption. The increase in total body oxygen consumption was met primarily by an increase in total body oxygen extraction during the development of fever. Cardiac index, heart rate, and systemic oxygen transport increased during the peak body-core temperature response. Systemic arterial blood pressure did not change significantly during the febrile response; however, pulmonic arterial blood pressure increased. During hypoxemia, peripheral vasoconstriction and shivering occurred following administration of SAE, but there was no change in total body oxygen consumption or body-core temperature. Thus, our data provide evidence that hypoxemia alters the febrile response of young lambs to bacterial pyrogen. The precise mechanism remains to be determined.

Animals↗
PubMedDate not supplied

Pyrogenic fever and blood plasma glucocorticoids after nonsteroid anti-inflammatory drugs.

Rabbits were injected with the lipopolysaccharide from E. coli (LPS) and received orally nonsteroid anti-inflammatory drugs (NSAIDs): acetylsalicylic acid, indomethacin, mefenamic acid, ibuprofen, aminophenazone, metamizole sodium, and phenylbutazone. These NSAIDs exerted antipyretic action without inhibiting the increase in the level of plasma glucocorticoids induced by LPS. This finding indicates the lack of correlation between the pyrogenic action of bacterial pyrogen and pyrogenic increase in the plasma glucocorticoid level. The investigated NSAIDs when given alone to normothermic rabbits differently affected the plasma glucocorticoid level: acetylsalicylic acid, indomethacin and ibuprofen depressed the plasma level of these hormones, mefenamic acid and phenylbutazone elevated it, and aminophenazone and metamizole sodium did not alter it significantly.

Animals↗
PubMed1978

[Effect of drugs on the pyrogenic reactivity of sheep].

Investigated was the effect of coffeine, bromine, atropine, and pilocarpine on the course of experimentally induced (by means of an Alcaligenes falcalis lipopolysaccharide) pyrogenic response in sheep. It was noted that coffeine aggravated, and bromine and partly atropine made more feasible the manifestation of the pyrogenic response in these animals. Pilocarpine enhanced some of the functions of the body while this reaction tookplace. Some arguments are given to elucidate the mechanism of the pyrogenic response.

Alcaligenes↗
PubMed1981

Differences of adrenal stress control mechanisms in subjects with glaucoma and normal subjects. Effect of vasopressin and pyrogen.

Various types of glaucomatous and normal subjects were tested for the adequacy of the stress response of their hypothalamic-pituitary-adrenal axis to pyrogen and vasopressin. With pyrogen, a significant response of elevation of plasma cortisol levels was positively correlated with ocular pressure and changes of the optic disc. Those subjects with increased ocular pressure and optic disc cupping and pallor had greater rises of plasma cortisol levels. With vasopressin, a decreased response of plasma cortisol levels was negatively correlated with the degree of elevated ocular pressure. Those subjects with increased ocular pressure and lower tonographic outflow facilities had smaller rises of plasma cortisol levels. Both tests indicated a disturbance of the hypothalamic-pituitary-adrenal axis in subjects with glaucoma.

Female↗
PubMed1993

Detection of streptococcal pyrogenic exotoxin genes by a nested polymerase chain reaction.

Severe invasive disease associated with group A Streptococcus (GAS) has recently increased in frequency. Isolates of GAS from normally sterile sites were examined for the streptococcal pyrogenic exotoxin genes spe A, spe B and spe C to determine if they play a role in this disease. Four primers for each gene were used in a nested polymerase chain reaction (PCR) configuration. The first PCR generated fragments of 818, 1106, and 801 bp, respectively, for the extotoxin genes. The second PCR generated fragments of 500, 912 and 654 bp for the spe A, spe B and spe C genes using the fragments from the first PCR as template. Of 62 strains tested, 35 (56%) contained the spe A gene, and 17 (27%) contained the spe C gene. All GAS strains studied, regardless of disease association, contained the spe B gene. These data corroborate accumulating evidence that the genes encoding pyrogenic exotoxin types B and C are not associated with severe invasive streptococcal illness including streptococcal toxic shock-like syndrome. This PCR-based gene detection system has clinical and epidemiologic applications because of its ease of performance, non-isotope labelling, high specificity and sensitivity, and lack of requirement for purified DNA.

Bacterial Proteins↗
PubMed1991

Pyrogenicity of polyadenylic.polyuridylic acid in rabbits.

Polyadenylic.polyuridylic acid injected intravenously into rabbits produced a rapid-onset, monophasic fever. Pyrogenic tolerance occurred in rabbits following daily injections of polyadenylic.polyuridylic acid. However, direct injection of the agent into the preoptic anterior hypothalamic region of rabbit's brain produced a markedly different fever. After an intrahypothalamic injection of polyadenylic.polyuridylic acid, fever was delayed in onset and persisted for a longer period. At room temperature, the fever was due to both increased metabolism and cutaneous vasoconstriction. In a colder atmosphere the fever was due solely to increased metabolism, whereas in the heat the fever was due to reduction in cutaneous blood flow and respiratory evaporative heat loss. In addition, the fever induced by intravenous polyadenylic.polyuridylic acid injection was reversed by a cyclooxygenase inhibitor, but not by a protein synthesis inhibitor. Polyadenylic.polyuridylic acid was shown to stimulate PGE2 production from rabbit's hypothalamus in vitro. The results reveal that this agent is a prostaglandin-dependent pyrogen.

Animals↗
PubMed1987

The effects of the protein synthesis inhibitor anisomycin on the febrile responses to intracerebroventricular injections of bacterial pyrogen, arachidonic acid and prostaglandin E2.

1. Anisomycin (15 mg/kg) was administered s.c. to cats at ambient temperatures of 5 degrees C, 20 degrees C and 38 degrees C. It produced biphasic effects on body temperature at 5 degrees C and 20 degrees C, an initial fall in temperature followed by a rise in body temperature, and a rise in body temperature of long latency at 38 degrees C. 2. Anisomycin (15 mg/kg) attenuated the hyperthermic responses to centrally injected PGE2 (1 microgram) at all ambient temperatures studied and also completely abolished the hyperthermic response to arachidonic acid (100 ng i.c.v.) at 20 degrees C. 3. Shigella dysenteriae (100 ng i.c.v.) raised the body temperature of cats by increasing heat production and reducing heat loss at 5 degrees C and 20 degrees C, and by increasing heat conservation at 38 degrees C. Anisomycin (15 mg/kg s.c.) pretreatment did not affect the temperature responses to the pyrogen at 20 degrees C and 38 degrees C, but did reduce the responses to Shigella dysenteriae (100 ng and 1 microgram i.c.v.) at 5 degrees C. 4. Anisomycin (15 mg/kg s.c.) was administered to cats, 90 min after the injection of Shigella dysenteriae (100 ng i.c.v.), at 20 degrees C at the onset of hyperthermia in control experiments. Under these conditions, no hyperthermia was observed over a 2 h period following anisomycin injection. 5. It is concluded that anisomycin interferes with pyrogen induced fever by acting at a site after PGE2 in the pathway to fever.

Animals↗
PubMed1991

Response of body temperature and serum iron concentration to repeated pyrogen injection in rabbits.

We measured body temperature and serum iron concentration after five daily consecutive injections of febrile doses of Salmonella typhosa lipopolysaccharide (0.1 micrograms/kg) and two doses of Staphylococcus aureus cell walls (1 x 10(7) and 5 x 10(7) cells) in rabbits. Tolerance to endotoxin injection, as manifest by a significant attenuation in the body temperature elevation, developed after the first injection of endotoxin. The endotoxin-induced fall in serum iron concentration was attenuated significantly by the 5th day of endotoxin injection. In contrast, no tolerance developed in either the body temperature or serum iron response following repeated daily injections of S. aureus. Rabbits rendered tolerant to endotoxin showed normal febrile and serum iron responses to subsequent S. aureus injection. Rabbits given serial injections of S. aureus, although not tolerant to S. aureus itself, exhibited attenuated body temperature responses but not serum iron responses to endotoxin injection. We suggest that repeated injection of endotoxin diminishes the ability of endotoxin to stimulate endogenous pyrogen (EP) synthesis and/or release, a property not shared by the gram-positive pyrogen S. aureus. However, repeated injection of S. aureus weakens the central endotoxin-EP pathway.

Animals↗
PubMed1976

The effect of an inhibitor of adenylate cyclase on the development of pyrogen, prostaglandin and cyclic AMP fevers in the rabbit.

An exotoxin of Bacillus thuringiensis known to inhibit adenylate cyclase in vitro has been used to investigate the role of cyclic AMP in the pathogenesis of fever in the rabbit. Intra-hypothalamic microinjections of the exotoxin are non-pyrogenic and significantly attenuate the hyperthermia caused by intrahypothalamic microinjections of both bacterial pyrogen (endotoxin) and prostaglandin E1. The hyperthermia produced by dibutyrl cyclic AMP is not affected by the exotoxin. These results support the idea that adenylate cyclase is activated during the development of fever in the rabbit.

Adenine Nucleotides↗
PubMed1976

Influence of endogenous pyrogen on the cerebral prostaglandin-synthetase system.

The biotransformation of arachidonic acid to prostaglandins in vitro is specifically augmented by endogenous pyrogen to a degree depending on the concentration applied, providing that the microsomal fraction of the cerebral cortex is used as prostaglandin-synthetase system. This effect is inhibited by non-steroidal anti-inflammatory agents. These findings are compatible with the hypothesis that prostaglandins might act as mediators of the febrile reaction induced by endogenous pyrogen.

Animals↗
PubMed1990

Interleukin-1 beta analogues with markedly reduced pyrogenic activity can stimulate secretion of adrenocorticotropic hormone in rats.

We examined the adrenocorticotropic hormone-releasing activities of several human interleukin-1 beta analogues that have markedly reduced pyrogenic activities in rats. Among the analogues tested, [Gly4]-, [Leu93]- and [1-148]-interleukin-1 beta increased the plasma adrenocorticotropic hormone level to almost that induced by authentic human interleukin-1 beta. Modifications of the N-terminus of the authentic molecule, i.e., [7-153]- and [Des-Ala1, Asp4]-interleukin-1 beta, significantly reduced the hormone-releasing activity. These data suggest that the adrenocorticotropic hormone-releasing activity of human interleukin-1 beta resides in the N-terminal structure of the authentic peptide and can be separated from its pyrogenic activity.

Adrenocorticotropic Hormone↗