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PubMed1987

Pyrogens fail to produce fever in the snakes Psammophis phillipsii and Lamprophis fuliginosus.

1. Preferred body temperature of five diurnal, Psammophis philipsii and three nocturnal, Lamprophis fuliginosus, snakes was measured in a thermal gradient chamber by indwelling colonic thermocouples, before and after injection of a variety of pyrogens. 2. The snakes achieved their preferred body temperature by moving up and down in the gradient chamber; it was about 33 degrees C for P. phillipsii and 25 degrees C for L. fuliginosus. 3. The snakes did not develop fever in response to any of the pyrogens, whether gram-negative or gram-positive in origin, either on the day of injection or on the subsequent day. 4. We believe that fever is rare amongst reptiles.

Animals↗
PubMed1987

Pyrogens fail to produce fever in the leopard tortoise Geochelone pardalis.

1. The body temperature of seven tortoises, Geochelone pardalis, was measured in a thermal gradient chamber, by indwelling thermocouples, after injection of various pyrogens. 2. The tortoises regulated their body temperature by moving in the chamber. 3. The tortoises did not develop fever in response to any of the pyrogens we tested. 4. The results support the contention that fever in reptiles is not ubiquitous.

Animals↗
PubMed1993

Changes in pre- or postsynaptic adrenergic mechanisms modify the thermoregulatory responses produced by pyrogen in rabbits.

1. Thermoregulatory responses to BHT 920, prazosin (PRA) and 6-hydroxydopamine (6-OHDA) were investigated in pyrogen (lipopolysaccharide Escherichia coli, LPS) treated rabbits. 2. All the compounds in question, despite their different selectivity for pre- or postsynaptic adrenergic structures, significantly reduced pyrogen fever. Antipyresis was associated with inhibition of the metabolic rate. 3. The role of adrenergic mechanisms in fever, with particular respect to those of postsynaptic alpha-2, is discussed.

Adrenergic alpha-Agonists↗
PubMedDate not supplied

Serum thyroxin levels during hyperthermia evoked in the monkey by intrahypothalamic injection of PGE1, 5-HT or pyrogen.

Serotonin (5-HT), prostaglandin E1 (PGE1) or a bacterial pyrogen (E. coli or S. typhosa) was microinjected in a volume of 1.0--1.5 microliter into the hypothalamus of the unanesthetized monkey to evoke a long-term hyperthermia. Samples of venous blood collected every 15 min, before, during and after each fever were analyzed by radioimmunoassay for plasma thyroxin levels. There was no statistically significant correlation between plasma thyroxin values and a given phase of the hyperthermic episode induced by the microinjections of 5--HT, PGE1 or bacteria. The possibility that an enhanced release of the thyroid hormone serves to sustain a long-term elevation in temperature evoked by a centrally acting pyrogenic substance is not supported.

Animals↗
PubMedDate not supplied

Central thermosensitivity during fever produced by intra-PO/AH and intravenous injections of pyrogen.

Squirrel monkeys with thermodes implanted in the preoptic/anterior hypothalamic (PO/AH) region and the medulla oblongata were used to examine three questions about central thermoresponsiveness in fever: Does thermoresponsiveness of the PO/AH region and medulla change during fevers caused by injection of bacterial endotoxin IV or directly into the PO/AH region? Does thermosensitivity of these brain regions determine the upper fever limit? Is thermoresponsiveness of the PO/AH region affected by local injections of salicylate? Changes in rectal temperature and oxygen consumption in response to heating and cooling the PO/AH region were reduced during fever caused by intra-PO/AH injections of bacterial endotoxin compared with changes produced during afebrile periods. PO/AH thermosensitivity was also reduced during fever caused by IV administration of bacterial pyrogen. Prolonged cooling of the PO/AH region or the medulla oblongata during fever produced by peripheral and central pyrogen injections did not cause rectal temperature (Tre) to rise above 41.1 degrees C although local heating reduced Tre or limited the fever maximum. From the latter result it is concluded that both pools of central thermoreceptors can limit maximal fever by reacting to local high temperature but that lowered temperature in neither region can raise Tre above a level determined by antagonistic input from thermoreceptors in other parts of the body. Injections of sodium salicylate into the PO/AH region had no effect on thermoresponsiveness of the region. This finding reinforces the idea that salicylates do not produce antipyresis by acting directly on thermosensitive cells of the central temperature control system.

Animals↗
PubMedDate not supplied

The role of protein synthesis in the hypothalamic mechanism mediating pyrogen fever.

The effects of inhibition of protein synthesis by anisomycin on the pathogenesis of fever and normal thermoregulatory processes were investigated in the conscious and unrestrained cat. Subcutaneous administration of 5.0-25.0 mg/kg of anisomycin prevented the fever normally evoked by an intravenous infusion of either 1.0 ml (10(8) organisms) of a 1:10 dilution of S. typhosa or 1.0-5.0 ml (3.5 x 10(5)-2.1 X 10(7) cells/ml) of endogenous pyrogen. In addition, systemic pre-treatment with anisomycin delayed and/or blocked the fever typically elicited by a direct micro-injection into the anterior hypothalamic, preoptic area (AH/POA) at AP 12.5-16.0 of 1.0 microliters of the endotoxin. Anisomycin did not alter the hyperthermic response to an anterior hypothalamic injection of either 1.0-7.0 micrograms/1.0 microliters of serotonin (5-HT) or 100.0 ng/1.0 microliters of prostaglandin (PGE). Inhibition of protein synthesis, furthermore, did not prevent the fall in body temperature usually produced by an intrahypothalamic micro-injection of 2.33-14.0 micrograms/1.0 microliters of either norepinephrine (NE) or dopamine (DA). The thermoregulatory capacity of the cat was unaffected by the administration of comparable doses of anisomycin, i.e., the animal was able to maintain normal body temperature (+/- 0.5 degrees C) when exposed to an ambient temperature of either 10 degrees C or 34 degrees C. These results strongly suggest that the synthesis of new protein within the region of the AH/POA is a functional requisite for the development of a pyrogen-induced fever.

Animals↗
PubMed1995

Congenital streptococcal toxic shock syndrome with absence of antibodies against streptococcal pyrogenic exotoxins.

Congenital infection with group A beta-hemolytic streptococcus was complicated by toxic shock syndrome in a neonate. We hypothesize that the severity of the clinical syndrome was related to the streptococcal pyrogenic exotoxin in the absence of corresponding antibodies. The outcome may have been favorably influenced by the antibodies to streptococcal pyrogenic exotoxin present in the immunoglobulins given as treatment.

Antibodies, Bacterial↗
PubMed1992

Role of the OVLT in the febrile response to circulating pyrogens.

The available data suggest that circulating endogenous pyrogens (EPs) probably do not penetrate the brain, but interact with sensory elements in the organum vasculosum laminae terminalis (OVLT) which may involve 5HT and SP as neurotransmitters. It is proposed that substance P (SP) may affect thermo-regulatory neurons in the preoptic area (POA) directly or induce the local synthesis of cytokines that secondarily act on these neurons. Recent evidence indicates that endothelial cells in the OVLT bind circulating cytokines to receptors on their luminal surface. This may result in the release of putative neuroregulators which then process the original signals inwardly to the POA, where they then affect neuronal functions leading to fever production. Thus, trans-BBB passage of cytokines is prevented, but the brain site mediating their pyrogenic effect is informed and the appropriate responses are activated. It is emphasized, however, that this suggested mechanism is still speculative.

Animals↗
PubMed1983

The preparation of pyrogen-free foetal calf serum for use in cell and tissue cultured.

A method is described for the preparation of foetal calf serum from blood drawn by heart puncture from calf foetuses obtained from a local municipal abattoir. This method differs from that previously described in that the Seitz Supra EK filter pads used in preliminary purification steps have been abandoned. These pads contain significant amounts of pyrogenic bacterial lipopolysaccharides and attempts to depyrogenate them with sodium hypochlorite, hydrogen peroxide and 1% foetal calf serum were unsuccessful. The modified method uses pyrogen-free glass fibre and cellulose fibre filters and provides an entirely satisfactory serum as proved by negative Limulus amoebocyte lysate tests and the excellent growth of cells.

Animals↗
PubMed1994

Separation of mitogenic and pyrogenic activities from so-called erythrogenic toxin type B (Streptococcal proteinase).

It is well-established that three types of erythrogenic toxins (ETA, ETB, ETC) are produced by Streptococcus pyogenes (group A streptococci) strains. Culture filtrate concentrates from Streptococcus pyogenes strains T19P (T19, ETA+, ETB+, ETC-), 27337 (T12, B3264, ETA-, ETB+, ETC+), 27252 (T4, ETA-, ETB+, ETC+) and 27195 (T8, ETA-, ETB+, ETC-) were analyzed by preparative isoelectric focusing. These concentrates and the purified erythrogenic toxin type B (ETB) isolated by ion exchange chromatography had mitogenic and pyrogenic activity. Now, it has been found that the mitogenic activity and the pyrogenic activity of this ETB can be separated by preparative isoelectric focusing in Sephadex gels. This means that ETB is not a superantigen as described in literature. The mitogenic and biological activity is caused by traces of ETA (strain T19P), ETC (strains 27252 and 27337) and/or by unknown mitogen(s) (MX, strain 27195) which preferentially stimulate V beta 8+ T cells. The differentiation between ETA (stimulating V beta 12+ but not V beta 8+ or V beta 2+), ETC (stimulating V beta 2+ but not V beta 8+), and MX (stimulating V beta 8+) was done using established leukemic cell lines.

Animals↗
PubMed1999

Sudden infant death syndrome: hypothalamic failure to sense elevated blood pyrogens.

Sudden infant death syndrome (SIDS) is frequently associated with a mild infection, the incidence peaking during the third month of life. We hypothesize that the neonatal immaturity of both the acute febrile response and hypothalamus promote neonatal protection from SIDS. Vagal afferents modify the febrile response. Vagotomized rodents displayed a loss of febrile responsiveness in a 'non-sensing' brain. The failure of a 'non-sensing' brain to react to elevated blood pyrogens leads to failure of the febrile response and to a shock-like state. SIDS infants may appear well yet, within hours of this observation, may be found dead. There is a mismatch between the acute febrile response and hypothalamic hypoactivation. The discrepancy increases with development. There is an elevated cytokine response in endothelial cells which induces nitric oxide (NO) production and retarded development of the hypothalamus. Cigarette smoke also induces NO production and retards hypothalamic development by augmented apoptosis. Zinc inhibits this effect in mouse thymocytes. Fetal haemoglobin (HbF) induces hypoxia, which is a stimulator of the immune response while vasodilator gases (carbon monoxide (CO), NO) reduce hypothalamic function. The hypothalamic failure to sense elevated blood pyrogens induces toxic shock - a feature of SIDS.

Animals↗
PubMed2000

Sudden infant death syndrome: hypothalamic failure to sense elevated blood pyrogens.

Sudden infant death syndrome (SIDS) is frequently associated with a mild infection, the incidence peaking during the third month of life. We hypothesize that the neonatal immaturity of both the acute febrile response and hypothalamus promote neonatal protection from SIDS. Vagal afferents modify the febrile response. Vagotomized rodents displayed a loss of febrile responsiveness in a 'non-sensing' brain. The failure of a 'non- sensing' brain to react to elevated blood pyrogens leads to failure of the febrile response and to a shock-like state. SIDS infants may appear well yet, within hours of this observation, may be found dead. There is a mismatch between the acute febrile response and hypothalamic hypoactivation. The discrepancy increase wtih development. There is an elevated cytokine response in endothelial cells which induces nitric oxide (NO) production and retarded development of the hypothalamus. Cigarette smoke also induces NO production and retards hypothalamic development by augmented apoptosis. Zinc inhibits this effect in mouse thymocytes. Fetal haemoglobin (HbF) induces hypoxia which is a stimulator of the immune response, while vasodilator gases (carbon monoxide (CO), NO) reduce hypothalamic function. The hypothalamic failure to sense elevated blood pyrogens induces toxic shock--a feature of SIDS.

Animals↗
PubMed1984

Specific absorption with monoclonal antibodies to muramyl dipeptide of the pyrogenic and somnogenic activities of rabbit monokine.

It is well established that muramyl dipeptide (MDP) can induce fever and enhance slow-wave sleep. Recently, crude or purified supernatants of activated macrophages containing endogenous pyrogen (EP) were also shown to enhance slow-wave sleep. These similarities and the recent finding that a mammalian factor that enhances slow-wave sleep is a muramyl peptide triggered us to study the possibility of the presence of this bacterial structure in the EP molecule. In the present study, EP was produced by stimulation of rabbit peritoneal cells with a nonpyrogenic, nonsomnogenic analog of MDP. The EP-containing supernatant lost its pyrogenicity and somnogenicity after passage over an immunoadsorbent column of monoclonal anti-MDP but not of another monoclonal antibody of different specificity. High percentage of the EP was recovered by elution of the anti-MDP columns with HCl/glycine buffer. Results suggest that bacterial muramyl peptides may be incorporated by mammalian cells into substances that act in picomole quantities to mediate immunological and physiological processes. In addition, the technique may be useful to extract interleukin 1 for structural studies.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1968

Studies on the pathogenesis of fever. XVI. Purification and further chemical characterization of granulocytic pyrogen.

Small quantities of highly purified granulocytic pyrogen have been separated from contaminating proteins by disc electrophoresis in polyacrylamide gel. The biologically active material thus isolated was shown to be electrophoretically homogeneous at pH 9 and pH 3.8. Earlier work on the chemical properties of the pyrogen molecule has been extended to include: (a) estimation of its molecular weight by gel filtration; (b) demonstration of free sulfhydryl groups essential for its biological activity; and (c) evidence that it is not inactivated by exhaustive extraction with ethanolether or n-heptane.

Animals↗
PubMed1970

Studies on the pathogenesis of fever. XVII. The cationic control of pyrogen release from exudate granulocytes in vitro.

Evidence has been presented that the release of active endogenous pyrogen from rabbit exudate granulocytes incubated in isotonic NaCl is a relatively prompt energy-dependent process that is preceded by a rise in intracellular pyrogen, and involves a rise in total intracellular cations and an increased permeability of the cell membranes, but does not require the synthesis of new proteins.

Animals↗
PubMed1977

Differences in pyrogen production by mononuclear phagocytes and by fibroblasts or HeLa cells.

Phagocytosis of bacteria stimulates "professional" phagocytes to produce and release endogenous pyrogen (EP), the protein that mediates fever. To determine whether "nonprofessional" phagocytes also have this capacity, mouse and human fibroblasts and HeLa cells were cultured after ingestion of latex or chicken erythrocytes (CE), and EP release into culture supernate measured by mouse assay. No detectable pyrogen was released by these cell types after phagocytosis, whereas both latex and CE stimulated EP production by cultured mouse macrophages. These studies support the hypothesis that only professional phagocytes of bone marrow origin synthesize EP and induce fever.

Animals↗
PubMed1979

Adherent cell function in murine T-lymphocyte antigen recognition. IV. Enhancement of murine T-cell antigen recognition by human leukocytic pyrogen.

A macrophage-dependent, antigen-specific murine T-cell proliferation assay was utilized to examine the role of soluble products of murine and human adherent cells in the activation of T lymphocytes. Highly purified human leukocytic pyrogen, and supernates from both murine and human mononuclear phagocytes-macrophages stimulated the immune T-cell proliferative response to the multideterminant antigens dinitrophenyl-ovalbumin and keyhole limpet hemocyanin. The implications of these studies and the relationship of leukocytic pyrogen to human lymphocyte-activating factor are discussed.

Animals↗