Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Administration of interleukin-1 (IL-1) induces increases in plasma ACTH and glucocorticoids. Numerous experiments have implicated the hypothalamic CRH neurosecretory system in these responses, but have failed to provide evidence for involvement of the ACTH secretagogue vasopressin (VP). The rat CRH neurosecretory system contains two types of cells: VP expressing and VP deficient. Hence, the above findings suggested that IL-1 may selectively activate the VP-deficient subtype of CRH neurosecretory cells. In this study we employed postembedding electron microscopic immunocytochemistry to directly assay IL-1-induced depletion of secretory vesicles from identified VP-expressing and VP-deficient CRH neurosecretory axons. IL-1-induced depletion of secretory vesicles from these axons was correlated with increases in plasma ACTH and decreases in plasma PRL. No dose of IL-1 was found that could selectively activate one subtype of CRH neurosecretory axons; at doses of 0.67 microgram/100 g and above for both IL-1 alpha and IL-1 beta, equal depletion of vesicles from the two subtypes was observed. Similar results were previously found after the injection of bacterial lipopolysaccharide, which induces the release of IL-1 from macrophages. The findings unequivocally establish for the first time that IL-1 activates hypothalamic CRH neurosecretory cells in the absence of surgical stress, anesthesia, disruption of the infundibular area, or administration of toxic drugs. In addition, these data clearly demonstrate that IL-1 induces the release of VP from neurosecretory axons in the portal capillary zone of the external zone of the median eminence. Previous studies have shown that the VP-deficient subtype of CRH neurosecretory axons is not strongly activated by several types of stress; therefore, activation of the system by inflammatory mediators involves mechanisms different from those mediating the stress response.
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PMID:Effects of interleukin-1 on the stress-responsive and -nonresponsive subtypes of corticotropin-releasing hormone neurosecretory axons. 131 22

The purpose of this research was to investigate whether the effects of regional anaesthesia on neutrophil migration differ from those due to general anaesthesia during major orthopaedic surgery in human patients. Eighteen patients underwent spinal or general anaesthesia (halothane or isoflurane) for surgery (six patients in each group). Blood samples were taken prior to induction of anaesthesia and after surgery was in progress for one hour. The movement of isolated neutrophils was measured in both samples in the chemotactic chamber toward lipopolysaccharide activated pooled serum. In addition plasma concentrations of catecholamines were determined in the blood samples. Neutrophils extracted from peripheral blood during spinal anaesthesia and surgery moved further towards a complement-derived attractant than neutrophils obtained from patients undergoing surgery under general anaesthesia with halothane or isoflurane and surgery (156.4 +/- 7.6 microns vs 114.3 +/- 6.1 microns or 119 +/- 8.4 microns respectively, P < 0.05). Increased concentrations of adrenaline were present in both general anaesthetic groups whereas the spinal group had lower concentrations than those prior to anaesthesia and surgery. It is considered unlikely that these differences in neutrophil reactivity are due to the direct effects of anaesthetic agents employed. The effects are likely to be the result of differing effects of spinal anaesthesia on the stress response or immunological mediators.
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PMID:Neutrophils from patients undergoing hip surgery exhibit enhanced movement under spinal anaesthesia compared with general anaesthesia. 145 Dec 16

Experiments were performed to investigate the vascular reactivity in both large and resistance artery preparations from an animal model of septic shock. New Zealand White rabbits were injected with a priming dose of Escherichia coli lipopolysaccharide (LPS), 15 micrograms/kg i.v., 18 hr before an i.v. dose of 200 to 2000 micrograms/kg under pentobarbital anesthesia. The second LPS challenge dropped mean blood pressure from 79 +/- 4 to 27 +/- 5 mm Hg in approximately 1 hr. At this time animals were sacrificed with the central ear arteries and kidneys being isolated for alignment in a Krebs-bicarbonate buffer perfusion apparatus to monitor perfusion pressure under constant flow conditions. Individual dose-response curves (DRCs) for norepinephrine (NE) and histamine were performed to assess contractile function. For examining vascular relaxant function, DRCs for methacholine (MC) and nitroprusside (NP) were conducted during a submaximal infusion of NE. The DRCs to NE and histamine were shifted to the right by 2- and 2.7-fold, respectively, in isolated ear artery preparations from LPS-treated vs. vehicle-treated animals. There was no difference in contractile function (using NE) in the two groups of perfused kidneys. The relaxation DRCs to MC were similar in the ear artery preparations from the two treatment groups whereas, in isolated kidneys, the relaxation to MC was significantly attenuated, by an average of 26 +/- 2% at each of six doses, in preparations from LPS-treated animals. The relaxation to NP was similar between the LPS- and vehicle-treated animals in the ear artery and kidney preparations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional differences in the effects of septic shock on vascular reactivity in the rabbit. 160 1

The progression to somatic death after brain death is poorly understood. The role of tumor necrosis factor (TNF) and interleukin-6 (IL-6) in this progression is unknown. TNF-like and IL-6-like plasma activities were assayed in a canine model of brain death in the presence and absence of a lipopolysaccharide (LPS) challenge (0.22 micrograms/kg). Bioassays for TNF-like and IL-6-like activities used WEHI and B9 cell lines, respectively. Brain death was induced by elevating and maintaining intracranial pressure above systolic arterial pressure. Anesthesia and the operative procedure did not cause a significant increase of either cytokine. Brain death (n = 8) itself did not cause a significant elevation of either cytokine compared with the sham brain-death control (n = 6) despite a significant decrease in mean arterial pressure (35 +/- 3 vs. 115 +/- 5 mmHg at 5 h). The brain-dead group treated with LPS (n = 6) responded with a significant elevation in IL-6-like and TNF-like activities compared with the vehicle-treated group. The rise of IL-6-like activity in response to LPS was greater in the brain-dead group than in the sham brain-dead group (n = 3); no significant difference was noted for the TNF-like response. We conclude that the progression to somatic death after brain death cannot be explained by increases in circulating TNF-like or IL-6-like activities.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma profiles of IL-6-like and TNF-like activities in brain-dead dogs. 195 61

The influence of sedative and anxiolytic benzodiazepines on human monocyte function was assessed in 11 patients undergoing anesthesia prior to control endoscopy of the urinary tract. A single i.v. injection of 0.08 mg/kg midazolam induced a marked and delayed inhibition of the lipopolysaccharide-induced production of interleukin-1 beta, tumor necrosis factor-alpha and interleukin-6 by monocytes isolated from peripheral blood. Corticosteroids were not responsible for the observed immunosuppression. These studies demonstrate that, when administered in man, benzodiazepines markedly alter the capacity of monocytes to synthetize major mediators of the host inflammatory response.
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PMID:Benzodiazepine anesthesia in humans modulates the interleukin-1 beta, tumor necrosis factor-alpha and interleukin-6 responses of blood monocytes. 195 61

The purpose of this study was to support the hypothesis that cytokines such as interleukin-1, tumor necrosis factor and interleukin-6 are released by macrophages or monocytes within 1 to 2 hr of phagocytosis of circulating, gut-derived bacterial lipopolysaccharide translocated by acute liver injury. Time courses of fever, neutrophilia and low blood-zinc levels generally attributed to cytokines were quantified after partial (67%) hepatectomy of rats under ether anesthesia. These acute phase responses in hepatectomized rats were compared with those after intravenous injection of exogenous endotoxin and human natural interleukin-1. Fever commenced 30 min after interleukin-1 injection, 4 hr after exogenous lipopolysaccharide injection and 6 hr after 67% liver resection. Similarly, rectal temperatures were significantly elevated in recipient rats 30 min after intravenous administration of donor plasma from hepatectomized animals, indicating that cytokines, not lipopolysaccharide, elicited the febrile response. Neutrophilia was present 1, 2, and 4 hr after interleukin-1 injection, lipopolysaccharide injection and hepatectomy, respectively. Furthermore, the reduction in plasma zinc, which depends on cellular metallothionein synthesis, occurred 4 hr after interleukin-1 administration and 6 hr after lipopolysaccharide injection or partial hepatectomy. Donor plasma from hepatectomized rats also elicited neutrophilia at 1 hr and low blood-zinc levels 4 hr after injection in recipient animals. The timing of these responses, just as for the fever, implies that cytokines and not lipopolysaccharide in the donated plasma elicited the neutrophilia and hypozincemia. Evidence was reviewed that interleukin-1, tumor necrosis factor and interleukin-6 function as hepatotrophic factors and have been identified in the circulation of humans with liver damage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute phase responses after acute liver injury by partial hepatectomy in rats as indicators of cytokine release. 211 49

Ventricle beta-adrenoceptors have been investigated and serum steroid levels determined in male rats injected intravenously with lipopolysaccharide from E. coli (LPS) under light anesthesia. Two series of doses were successively studied: 1) 2 and 3 mg.kg-1 and 2) 1 and 4 mg.kg-1, each including controls. The second series was carried out owing to the unexpected results of the first one. Homogeneity of the two series was tested. Experiments were performed at hr 4 after injection, a time previously tested to induce hormonal variations and release of a cardiodepressant factor (CDF) in serum. The results indicate that 2 mg.kg-1 LPS induced an increased activity of adenylate cyclase. The unexpectedly high response was dose-dependent since it was not found with the lowest or highest doses. The determination of serum steroid levels (progesterone, 17 alpha-hydroxyprogesterone, corticosterone, delta 4-androstenedione, testosterone, estrone, and estradiol) was used as a kind of marker of endotoxin activity. The results point out that the light anesthesia used for LPS injection delayed the hormonal response, when compared with results previously obtained with the same LPS dose (2 mg.kg-1) in unanesthetized rats. It can be inferred that the present data should usually appear at an earlier stage. It is suggested that an endotoxin-induced protein kinase C activation could be involved in the observed hyperactivity of adenylate cyclase and the hyperdynamic phase of septic shock.
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PMID:Unexpected hyperactivity of myocardial adenylate cyclase system in endotoxic male rats. 219 14

Observations were made on the differences in cell-mediated immune responses in the mice infected with strongly pathogenic Naegleria fowleri ITMAP 359, weakly pathogenic Naegleria jadini 0400, or non-pathogenic Naegleria gruberi EGB, respectively. Variations in cell-mediated responses and changes in antibody titers according to the duration after infection were noted. Infections were done by dropping 5 microliters saline suspension containing 10 x 10(4) trophozoites cultured axenically in the CGVS medium into the right nasal cavity of ICR mice aging about 6-7 weeks, under the anesthesia by intraperitoneal injection of secobarbital. Following infection, delayed type hypersensitivity(DTH) responses in the footpad and blastogenic responses of the mouse spleen cells using [3H]-thymidine were observed on the day 1, 4, 7, 10 and 14 after infection. For the preparation of amoeba lysates, each of cultured trophozoites were homogenized with an ultrasonicator, and centrifugated at 20,000 g. The supernatants of amoeba lysates were used as the mitogen and antigen for ELISA. Concanavalin A(Con. A) and lipopolysaccharide(LPS) were also used as mitogens in the blastogenic response. 1. The mice infected with N. fowleri showed the mortality rate of 75.7%. The rate was 6.2% for the N. jadini infected group, while no dead mouse was observed for N. gruberi infections. 2. In regard to DTH responses in the N. fowleri infected mice, the level increased in comparison to the control group but declined after 7 days. An increase was also noted for the N. jadini group after 1 day, but gradual decreases were observed through the infection period. In addition, no difference was noted between the N. gruberi infected and control groups. 3. Concerning the blastogenic response of the splenocytes, it increased after 10 days in the experimental group of N. fowleri infection, but the differences were not statistically significant compared with control group. It was evident that N. jadini group was not different from control group either, while there was a tendency of decrease in N. gruberi infected group. In regard to the blastogenic response of the splenocytes by LPS, it was found that the N. fowleri, N. jadini and N. gruberi infected groups had no differences from the control group. 4. The serum antibody titer of N. fowleri and N. jadini infected mice increased from the day 7 and 14 after infection respectively, while the N. gruberi infected mice showed no increase.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Studies on the cell-mediated immunity in experimental Naegleria spp. infections]. 248 28

For much of the last decade, an increasing number of surgeons have been interested in objective assessment of cellular contributors to host defense function. In order to study many of these processes, it is apparently desirable that the cells be isolated to the extent feasible for the purpose of analyzing a more or less pure population of cellular elements. The purpose of this paper is to describe the physiologic activation of mononuclear cells that occurs as a result of the isolation process. Therefore, it follows logically that such cells are therein intrinsically less responsive to further physiologic manipulation in vitro. Analyses of such data without an awareness of this intrinsic aberration will undoubtedly lead to misinterpretation of the capacity of such cells for further modulation by immunostimulants or by the intrinsic processes related to injury, anesthesia, and operation. Furthermore, it may indicate that certain agents, e.g., cytokines, are unable to stimulate cellular function when, in fact, the defense function of the cell has been initially stimulated by the isolation procedure. Fractionation of human peripheral blood over Hypaque-Ficoll and subsequent purification of monocytes by adherence to plastic lead to an increase in the relative density of HLA-DR on monocytes. This increase occurred when carried out in endotoxin lipopolysaccharide (LPS)-contaminated or LPS-depleted reagents. LPS, added experimentally to whole blood, enhanced HLA-DR expression on monocytes without further manipulation. Monocyte HLA-DR expression measured in whole blood was reduced in patients with major sepsis (n = 19) compared to normal subjects (n = 10).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Experimental and clinical significance of endotoxin-dependent HLA-DR expression on monocytes. 273 99

We studied the effects of superoxide dismutase (SOD), an enzyme that converts superoxide into peroxide, on the cardiopulmonary response to endotoxin in sheep. Sheep (n = 18) were prepared for chronic measurement of cardiopulmonary variables, including lung lymph flow, by surgically implanting catheters under halothane anesthesia. Nine of the animals were studied before and after the administration of endotoxin (0.75 microgram/kg) with and without SOD. An additional nine animals received SOD without the lipopolysaccharide. Endotoxin produced an increase in lung lymph flow that was initially associated with a marked pulmonary arterial (PA) hypertension and reduced lymph-to-plasma protein ratio (L/P). The lymph flow remained elevated later in the response, but there was only a mild increase in PA pressure, and the L/P was normal. There was also a fall in blood neutrophils and in cardiac index. SOD increased this secondary elevation in lung lymph flow, and the corresponding L/P was greater than the preendotoxin value. The fall in neutrophil count, cardiac output, and the elevation in PA pressure seen with endotoxin were not affected by SOD. When administered in the absence of endotoxin, SOD produced no perceptible change in the cardiopulmonary and lymph values. We conclude that peroxide, hydroxyl ion, and/or other free radicals formed by the action of SOD must be responsible for a portion of the endotoxin response rather than superoxide itself.
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PMID:Potentiation of lung vascular response to endotoxin by superoxide dismutase. 398 Mar 70


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