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)

Cachectin-tumor necrosis factor (TNF-alpha) has been implicated as a possible signal for the initiation of human parturition in the setting of infection. These studies were conducted to determine whether human decidua can produce TNF-alpha in response to bacterial lipopolysaccharide (LPS). Decidual explants from women undergoing elective cesarean sections were incubated with and without Escherichia coli LPS (25 ng/ml) for 20 h. TNF-alpha concentration in the conditioned media was measured with an enzyme-linked immunoassay and bioassay (L929 bioassay). While conditioned media from unstimulated decidual explants contained either undetectable or low levels of TNF-alpha, conditioned media from LPS stimulated decidua contained TNF-alpha (mean = 2.6 pmol/mg protein per 20 hours, SEM +/- 1.03). There was a strong correlation between the immunoreactive and bioactive TNF-alpha (Spearman rank correlation r = 0.76, P less than 0.001). We conclude that human decidua in vitro can produce TNF-alpha in response to LPS.
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PMID:Human decidua: a source of cachectin-tumor necrosis factor. 193 92

The effects of cryopreservation on bacterial lipopolysaccharide (LPS)-induced interleukin-1 (IL-1) production by unfractionated mononuclear cells (MNCs), adherent cells (ACs), and nonadherent cells (NACs) were studied. Culture supernatants from cryopreserved cells contained significantly larger concentrations of IL-1 [MNCs, 211 +/- 50; ACs, 640 +/- 41; NACs, 116 +/- 19 U/ml (mean +/- SEM)] as compared with supernatants from fresh cells (69 +/- 22, 427 +/- 69, and 72 +/- 33 U/ml, respectively). In addition, supernatants obtained from cocultures of autologous fresh and frozen cells contained much less than the expected quantities of IL-1 (78 +/- 8%), indicating that suppressor cells in the fresh population are responsible for the decreased IL-1 content. The studies suggest that functional inactivation of cryosensitive suppressor monocytes is associated with an increase in IL-1 production by the other subset. The results provide further evidence that lack of active suppressor monocytes and increased IL-1 production may be responsible for the previously reported enhanced plaque-forming cell responses of cryopreserved cells from normal controls and from patients with lung cancer.
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PMID:Cryopreservation enhances interleukin-1 production in human mononuclear cells. 213 99

Peripheral blood monocytes were obtained from 19 patients with cystic fibrosis (CF) and age-matched paired normal individuals. The oxidative metabolic response of these cells was measured by superoxide anion production before and after stimulation with Salmonella typhimurium or Pseudomonas aeruginosa lipopolysaccharide (LPS). CF monocytes showed slightly greater spontaneous superoxide anion production (14.1 +/- 2.1 SEM nanomoles superoxide anion/10(6) monocytes/180 min; n = 12) than normal monocytes (9.5 +/- 1.4; n = 12), P = 0.009. No differences between CF and normals were found in LPS-stimulated superoxide anion production (CF = 33.5 +/- 4.6, n = 13; normal = 33.8 +/- 4.2, n = 13). Furthermore, CF monocytes responded to both P. aeruginosa and S. typhimurium LPS stimulation as well as to recombinant interferon-gamma. Superoxide anion production of CF monocytes was comparable in autologous serum and in normal serum, and responses of patients colonized with P. aeruginosa and P. cepacia did not differ. We conclude that CF monocytes have a slightly increased metabolic level and, despite chronic infection, are capable of a further response to exogenous microbial stimuli.
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PMID:Monocytes in cystic fibrosis: responsiveness to microbial stimuli. 216 9

Alveolar macrophages contribute to acute pulmonary inflammation by secretion of neutrophil chemoattractants. We determined if one of these attractants is neutrophil attractant/activating protein (NAP-1), which is secreted by blood monocytes stimulated by lipopolysaccharide (LPS). Alveolar macrophages were stimulated in tissue culture with 10 micrograms/ml LPS. Culture fluids collected at 24 h were assayed for both neutrophil chemotactic activity and the concentration of NAP-1 as determined by a sandwich ELISA. The concentration of NAP-1 in culture fluid to LPS-stimulated macrophages was 860 +/- 40 ng/ml (SEM for six normal subjects). NAP-1 in fluid of unstimulated macrophages was 40 +/- 15 ng/ml. We confirmed the presence of NAP-1 in culture fluid of LPS-stimulated lung macrophages by immunoaffinity and HPLC-CM column purification. The HPLC-CM elution profile of macrophage NAP-1 was identical to that of monocyte NAP-1, and the N-terminal sequence of the protein in one of the isolated peaks corresponded to that of monocyte-derived NAP-1 beta. Two lines of evidence show that NAP-1 does not account for all neutrophil chemotactic activity in culture fluid of 24-h, LPS-stimulated macrophages. At a dilution of culture fluid that elcited the same chemotactic response as a known concentration of pure NAP-1, the concentration of culture fluid NAP-1 was only one-tenth that of pure NAP-1. (ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Secretion of neutrophil attractant/activation protein by lipopolysaccharide-stimulated lung macrophages determined by both enzyme-linked immunosorbent assay and N-terminal sequence analysis. 217 29

Interleukin-6 (IL-6) is produced by various cell types, including monocytes, fibroblasts, and endothelial cells. IL-6 has also been detected in the urine of normal and renal transplant patients. Thus, the possible production of this cytokine by glomeruli and mesangial cells was investigated. Rat glomeruli were obtained by serial sieving of cortical homogenates of blood-free kidneys. Mesangial cells were obtained from the glomeruli and cultured under standard methods in RPMI 1640 medium containing 15% fetal calf serum. Glomeruli or confluent monolayers cells were then incubated in RPMI 1640 for 18 hr, in the presence or not of tumor necrosis factor-alpha (TNF alpha), lipopolysaccharide (LPS), or platelet-activating factor (PAF). IL-6 activity was measured using the IL-6-dependent cell line subclone (B 9-9) and expressed with respect to a standard curve established with recombinant IL-6. Glomeruli generate IL-6 upon TNF alpha (100 ng/ml) and LPS (1 microgram/ml), 11,500 +/- 3000 and 22,000 +/- 7500 U/ml, respectively. Nonstimulated mesangial cells produced 50 +/- 5 U/ml (mean +/- SEM, n = 4) of IL-6. TNF alpha (1 ng/ml) and LPS (1 microgram/ml) induced the production of 800 +/- 90 and 40,000 +/- 5000 U/ml, respectively (n = 4). In contrast, PAF (0.1 nM-1 microM) did not increase IL-6 production from glomeruli or mesangial cells. These results demonstrate that renal cells spontaneously generate minimal amounts of IL-6 and that this production is significantly increased by TNF alpha or LPS. A synergy between LPS and TNF alpha was induced in glomerular cells with 10 ng/ml of TNF alpha and graded concentrations of LPS. Thus, the production of IL-6 by glomerular cells and its modulation by other cytokines or endotoxins may play a role in the local immunological processes leading to immune glomerular diseases.
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PMID:Interleukin-6 production by tumor necrosis factor and lipopolysaccharide-stimulated rat renal cells. 219

A thymocyte proliferative response assay was used to compare spontaneous and lipopolysaccharide (LPS)-induced interleukin-1 (IL-1) release by alveolar macrophage (AM) in asthmatic patients and normal subjects. Twelve asthmatic patients and seven nonsmoking healthy subjects underwent a bronchoalveolar lavage (BAL). All asthmatic patients had a reversible airway obstruction and 7/12 were allergic. BAL AM were separated by adherence on tissue culture plates in medium RPMI-1640 supplemented with antibiotics and fetal calf serum, and were incubated with or without 10 micrograms/ml LPS for 20 h. Free-cell supernatants were tested by C3H/HeJ mice thymocyte proliferative assay. Unstimulated AM supernatant IL-1 activity was significantly higher in asthmatic patients (mean +/- SEM: 47.8 +/- 11.9 units/10(6) AM) in comparison with healthy subjects (4.8 +/- 2.3 units/10(6) AM; p less than 0.05, Mann-Whitney U test) but did not significantly differ between allergic (42.2 +/- 15.5 units/10(6) AM) and intrinsic asthmatic patients (55.8 +/- 20.7 units/10(6) AM). For healthy subjects, IL-1 activity was significantly higher in LPS-stimulated AM supernatants (85 +/- 20 units/10(6) AM, p less than 0.05; Mann-Whitney U test) in comparison with unstimulated ones; for asthmatic patients, unstimulated and LPS-stimulated AM supernatant IL-1 activity did not significantly differ. This finding is in accordance with previous work suggesting that AM from asthmatic patients have a weak suppressive activity upon lymphocyte proliferation and emphasize the enhanced AM releasability in asthma.
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PMID:Interleukin-1 release by alveolar macrophages in asthmatic patients and healthy subjects. 234 Dec 2

We examined the functional importance of immunoglobulin polypeptide fragments generated by Pseudomonas aeruginosa elastase (Pseudomonas elastase). The purpose of this study was to determine whether the elastase produced by Pseudomonas aeruginosa cleaves human IgG into immune fragments that functionally inhibit opsonophagocytosis. Our results confirm that IgG isolated from patients with cystic fibrosis (CF) incubated with purified pseudomonas elastase results in the generation of two major polypeptide fragments and that, furthermore, these fragments significantly inhibit bacterial uptake by human neutrophils. After 75 minutes bacterial uptake was six times greater when intact IgG was used as an opsonin (uptake 90.2% +/- 18.6% SEM) compared with a IgG was used as an opsonin (uptake 90.2% +/- 18.6% SEM) compared with a mixture of pseudomonas-lipopolysaccharide-reactive Fab and F(ab')2 fragments generated by pseudomonas elastase (uptake 15.4% +/- 0.8% SEM, p less than 0.001). Hydrolyzed CF IgG antibodies consistently resulted in a level of bacterial uptake less than that of normal saline negative controls (NS): (at 10 minutes, NS 26.6% vs CF 16.8%, p less than 0.05; at 75 minutes, NS 28.2% vs CF 15.4%, p less than 0.01. This suggests that the immune polypeptides are active inhibitors of the essential neutrophil phagocyte-bacterial cell interaction. Intact immune IgG reversed the defect in opsonophagocytosis. When intact IgG was mixed with IgG fragments the phagocytic rates increased directly with increasing amounts of intact IgG. We conclude that the elastase exoproduct secreted by Pseudomonas aeruginosa is capable of cleaving IgG into functionally important fragments that inhibit bacterial uptake. Furthermore, this inhibition can be overcome by increasing amounts of a commercially available preparation of intact immune IgG.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Functional importance of cystic fibrosis immunoglobulin G fragments generated by Pseudomonas aeruginosa elastase. 251 65

In this study we assessed the viability of cultured human umbilical vein endothelial cells (HUVE) treated with bacterial lipopolysaccharide (LPS), recombinant human interleukin-1 (rhIL-1), or recombinant human tumor necrosis factor-alpha (rhTNF-alpha) during inhibition of RNA or protein synthesis. Cytotoxicity was determined by 51Cr activity retained in labeled HUVE monolayers after exposure to LPS, rhIL-1 or rhTNF-alpha, and cycloheximide (Cx) or actinomycin D (Act D). Lipopolysaccharide (150 ng/ml), rhIL-1 (100 pg/ml), or rhTNF-alpha (20 ng/ml) alone was not toxic to HUVE in an 18-hr incubation. Cycloheximide alone (1 microgram/ml for 18 hr) or Act D alone (1 microgram/ml for 6 hr) was also not toxic to HUVE. However, coincubation of HUVE with Cx and LPS (150 ng/ml), rhIL-1 (10 pg/ml), or rhTNF-alpha (20 ng/ml) produced significant cytotoxicity at 18 hr (70 +/- 4% for LPS, 75 +/- 5% for rhIL-1, and 52 +/- 5% for rhTNF-alpha; mean +/- SEM of 18, 16, and 19 separate experiments, respectively). Similarly, coincubation of HUVE with Act D and LPS, rhIL-1, or rhTNF-alpha resulted in 82 +/- 5%, 85 +/- 3%, and 67 +/- 4% cytotoxicity, respectively, at 6 hr (mean +/- SEM of 5 separate experiments for LPS, and 7 separate experiments each for rhIL-1 and rhTNF-alpha). At the highest concentrations of LPS, rhIL-1, or rhTNF-alpha, cytotoxicity during coincubation with Cx or Act D was detected as early as 2 hr and was near maximal by 6 hr. In contrast to LPS, rhIL-1, or rhTNF-alpha, recombinant human interferon-gamma (up to 100 U/ml), or human alpha-thrombin (up to 10 U/ml), produced no cytotoxicity in the presence of Cx. Recombinant human lymphotoxin (up to 50 ng/ml) had a detectable cytotoxic effect in the presence of Cx although it was significantly less than that seen with rhTNF-alpha. Furthermore, coincubation of human fibroblasts and human smooth muscle cells with Cx and LPS, rhIL-1, or rhTNF-alpha produced no cytotoxicity. We conclude that under these culture conditions, LPS, rhIL-1, or rhTNF-alpha produces a lethal injury to HUVE when de novo RNA or protein synthesis is inhibited. These results suggest that LPS, rhIL-1, and rhTNF-alpha may act via a common pathway in endothelial cells and that protein synthesis is important in regulating the response to these stimuli.
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PMID:Human endothelial cell response to lipopolysaccharide, interleukin-1, and tumor necrosis factor is regulated by protein synthesis. 278 80

Serologic recognition of common lipopolysaccharide core antigens has been related to enhanced resistance to gram-negative bacterial disease in several species. Class-specific titers (IgG, IgM) were determined by direct ELISA, using intact Escherichia coli (J5) as a plate antigen. Serum samples were obtained from 224 neonatal swine between the ages of 36 and 60 hours. The mean (+/- SEM) log10 IgG titer against gram-negative core antigens was 1:1,713 +/- 0.4718 and the mean log10 IgM titer was 1:202 +/- 0.5644. The IgG titer was directly related with litter size, birth weight, and serum total IgG concentration; IgM titer was directly related with dam parity and serum total IgG concentration.
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PMID:Humoral recognition of lipopolysaccharide core antigens of gram-negative bacteria in neonatal swine. 291 17

Lipopolysaccharide (10 micrograms/ml) was found to stimulate resident mouse peritoneal macrophages to produce leukotriene C4 (36 +/- 1.3 ng/10(6) cells, SEM, n = 20) within 16 h. Spontaneous synthesis in control cultures without lipopolysaccharide was less than 1.6 ng/10(6) cells. Leukotriene C4 was characterized by reversed-phase high-performance liquid chromatography, ultraviolet spectrometry and radioimmunoassay. When the macrophages, prelabeled with [3H]arachidonic acid, were treated with lipopolysaccharide radioactivity was incorporated into leukotriene C4. The amount produced varied with the method of macrophage preparation and incubation conditions and was dependent on the amount of lipopolysaccharide added (0.5-60 micrograms/ml), on cell counts and on the incubation time (4-16 h). The released leukotriene C4 was converted to a compound identified as a C6-cysteinylleukotriene, indicating metabolism of the leukotriene by the macrophages. Parallel determinations of prostaglandins E2 and F2 alpha by radioimmunoassay demonstrated that leukotriene C4 and prostaglandin E2 are formed by mouse peritoneal macrophages to a similar degree.
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PMID:Formation and metabolism of leukotriene C4 in macrophages exposed to bacterial lipopolysaccharide. 308 25


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