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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A single intravenous injection of 5 micrograms of Yersinia enterocolitica lipopolysaccharide (LPS) inhibits rabbit polymorphonuclear leucocyte (PMN) chemotaxis, enzyme secretion, and respiratory burst activation in response to partially purified rabbit C5a and leucotriene B4 (LTB4). Respiratory burst activation is also inhibited in response to platelet activating factor (PAF). In contrast, all these responses to n-formyl-methionyl-leucyl-phenylalanine (FMLP) remain unaltered. This LPS does not modulate PMN activation in vitro or activate the respiratory burst. Thus Y enterocolitica LPS acts in vivo by inhibiting PMN responses to endogenous mediators of inflammation. This inhibition presumably impairs the elimination of pathogens and might, therefore, provide favourable conditions for induction by bacteria of further immunological consequences.
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PMID:Inhibition of polymorphonuclear leucocyte functions in vivo by Yersinia enterocolitica lipopolysaccharide. 253 4

Glucocorticoids exert their actions through a time-dependent, receptor-mediated, protein synthesis- and RNA synthesis-dependent mechanism. We have assessed the effects of 24-h culture of human neutrophils with dexamethasone on degranulation, chemotaxis, binding to vascular endothelium and formation of leukotriene B4. Purified neutrophils contained an average of 2896 [3H]dexamethasone binding sites per cell with a Kd of 4.1 X 10(-9) M for [3H]dexamethasone binding. Cells exposed to dexamethasone (10(-6) M) released equal or greater quantities of the lysosomal enzymes, lysozyme and beta-glucuronidase in response to formylmethionyl-leucyl-phenylalanine, serum activated zymosan, and the tumor promoting phorbol diester 12-O-tetradecanoylphorbol-13-acetate compared to controls. Culture with dexamethasone also did not inhibit neutrophil chemotaxis in response to a range of concentrations of formylmethionyl-leucyl-phenylalanine, or did it inhibit binding of neutrophils to cultured endothelial cells stimulated by either leukocyte activators (formylmethionyl-leucyl-phenylalanine and platelet-activating factor) or endothelial activators (interleukin-1, lipopolysaccharide or 12-O-tetradecanoylphorbol-13-acetate). Spontaneous adherence of neutrophils to endothelial cells was inhibited (82.9 +/- 6.8% of control, P less than .025, n = 18). Neither in vitro or in vivo glucocorticoids inhibited neutrophil leukotriene B4 formation induced by either the calcium ionophore A23187 or serum activated zymosan. We conclude that human neutrophils are not functionally inactivated by glucocorticoids and suggest that the mechanism by which glucocorticoids inhibit neutrophil accumulation at inflammatory sites may be by inhibition of the production of chemoattractants and endothelial activators rather than inhibition of their actions.
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PMID:An assessment of the effects of glucocorticoids on degranulation, chemotaxis, binding to vascular endothelium and formation of leukotriene B4 by purified human neutrophils. 254 40

Plasma endotoxin concentrations and oxidative burst response of peripheral blood polymorphonuclear leukocytes were examined in 12 patients undergoing coronary artery bypass. The measurements were made just before the operation, 5 minutes after removal of the aortic crossclamp, and 24 hours after the operation. Endotoxin was quantitated by a combination of a sensitive Limulus amebocyte lysate assay and rocket immunoelectrophoresis measuring picogram amounts of endotoxin. Peripheral blood neutrophils were purified by a two-step dextran sedimentation and metrizoate sodium Ficoll (Lymphoprep., Nyegaard, Oslo, Norway) centrifugation. The oxidative burst response of these cells was measured for their ability to generate superoxide anion and was determined by a cytochrome c reduction assay. Preoperatively, all the plasma samples except one were free of endotoxin. The endotoxin levels reached 100 pg/ml 5 minutes after removal of the aortic crossclamp, and except in one sample they had decreased 24 hours after the operation. Studies on the generation of superoxide by neutrophils showed a decline in the response 5 minutes after removal of the aortic crossclamp and an enhancement of the response to f-Met-Leu-Phe by cells obtained from 11 of 12 patients 24 hours postoperatively. In vitro addition of bacterial lipopolysaccharide to blood from healthy individuals also enhanced the superoxide response of the neutrophils. We conclude that during cardiopulmonary bypass the circulating blood is contaminated by endotoxin and the neutrophils are primed for enhanced generation of oxygen radicals. The released oxygen radicals may be involved in the tissue damage observed in these patients.
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PMID:Endotoxemia and enhanced generation of oxygen radicals by neutrophils from patients undergoing cardiopulmonary bypass. 254 7

Murine bone marrow-derived macrophages (BMM) undergo DNA synthesis in response to growth factors such as colony stimulating factor-1 (CSF-1) and granulocyte-macrophage CSF (GM-CSF). These macrophages can also be "activated," but without subsequent DNA synthesis, by a number of other agents, including lipopolysaccharide (LPS), concanavalin A, zymosan, formyl-methionyl-leucyl-phenylalanine (FMLP), and the Ca2+ ionophore, A23187. When BMM are treated with a range of stimuli, there is some, although not perfect, correlation between transient elevations in both c-myc mRNA and c-fos mRNA levels and increases in DNA synthesis. However, enhanced DNA synthesis and oncogene expression are readily dissociated from rises in inositol phosphates and, by implication, phospholipase C-mediated hydrolysis of phosphatidyl inositol 4,5-bisphosphate. Superoxide formation in BMM can also be dissociated from the other responses and does not necessarily depend on protein kinase C activation.
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PMID:Activation and proliferation signals in murine macrophages: relationships among c-fos and c-myc expression, phosphoinositide hydrolysis, superoxide formation, and DNA synthesis. 255 11

I describe the effect on phagocytic activity of the migration of bovine blood polymorphonuclear leukocytes (PMNL) through collagen and a monolayer of PK-15 cells in vitro infected with rotaviruses (strain OSU, RFC-17, SA-11), a picornavirus (strain SVDV), bovine herpesvirus (BHV-1) and equine herpesvirus (EHV-1). The PMNL were examined before and after their migration as follows: (1) for EA rosette formation with sensitized sheep erythrocytes, (2) for phagocytic activity mediated through Fc receptors (FcRs), (3) for phagocytic activity mediated through immunologically nonspecific receptors (INsRs). Random migration of PMNL through the infected monolayer to RPMI-1640 medium containing or lacking chemotactic agents (zymosan activated serum--Act. serum) and/or containing control agents (lipopolysaccharide--LPS or formyl-L-methionyl-L-leucyl-L-phenylalanine--fMLP) decreased the percentage of rosettes forming PMNL and the phagocytosis mediated by FcRs and INsRs. The results obtained suggest that the viruses used in this study independently of their biological properties exerted a suppressive action on the phagocytic activity mediated by FcRs and INsRs.
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PMID:Effect of viral infection of Fc receptors and immunologically nonspecific receptors of blood polymorphonuclear leukocytes: an in vitro model. 256 5

We examined the mechanisms involved in neutrophil adherence to cultured human umbilical vein endothelial cells (HEC) induced by direct stimulation of the neutrophils by phorbol myristate acetate (PMA), formylmethionyl-leucyl-phenylalanine (FMLP), or the calcium ionophore A23187 (neutrophil-dependent adherence), or by pretreatment of HEC with interleukin-1 (IL-1), tumour necrosis factor (TNF) or lipopolysaccharide (LPS) (endothelial-dependent adherence). Two distinct mechanisms for neutrophil adherence to HEC were demonstrated by performing adherence assays: (i) at 37 degrees versus 4 degrees; (ii) in the presence of Ca2+ only versus Mg2+ only; and (iii) in the presence or absence of monoclonal antibodies (mAb) to the CD11/CD18 adhesion complex of neutrophils. A CD11/CD18-dependent mechanism (i.e. inhibited by anti-CD18 mAb) was identified that was active in the presence of Mg2+ only but not of Ca2+ only, and at 37 degrees but not at 4 degrees. A CD11/CD18-independent mechanism (i.e. not inhibited by anti-CD18 mAb) was active at 4 degrees and at 37 degrees, and in the presence of Ca2+ only and of Mg2+ only. Neutrophil-dependent adherence induced by FMLP or PMA occurred solely via the CD11/CD18-dependent mechanism, whereas endothelial-dependent adherence induced by a 4-hr pretreatment with IL-1, TNF, or LPS involved both CD11/CD18-dependent and/independent mechanisms. CD11/CD18-deficient neutrophils isolated from a patient with leucocyte adherence deficiency (LAD) maintained the ability to adhere to LPS-pretreated HEC in the presence of Ca2+ only, indicating that this mechanism of adherence involves a receptor on the neutrophil distinct from CD11/CD18. Furthermore, the disappearance of the CD11/CD18-independent, but not of the CD11/CD18-dependent mechanism of adherence, in HEC treated with TNF for 24 hr suggests that the two mechanisms of neutrophil adherence also involve distinct inducible endothelial-leucocyte adhesion molecules (E-LAM).
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PMID:CD11/CD18-independent neutrophil adherence to inducible endothelial-leucocyte adhesion molecules (E-LAM) in vitro. 257 36

Phagocytic activity and intracellular killing of opsonized staphylococci (Smith strain) by bovine blood polymorphonuclear leukocytes (PMNL) was studied after their migration in vitro in blind well chambers. The results indicate that migration of PMNL to RPMI-1640 medium without chemotactic factor significantly (P less than 0.01) increased the percentage of rosette-forming PMNL (from 11 +/- 2 to 49 +/- 4%), as well as phagocytic activity mediated through Fc receptors (FcRs) (from 25 +/- 3 to 81 +/- 4% phagocytizing PMNL and from 151 +/- 22 to 942 +/- 54 number of phagocytized staphylococci/100 PMNL), and intracellular killing of bacteria (from 13 +/- 2 to 59 +/- 7%). On the other hand, PMNL migration to RPMI-1640 medium with the chemotactic factor (serum activated with zymosan [AS] or lipopolysaccharide [LPS] or formyl-L-methionyl-L-leucyl-L-phenylalanine [fMLP]) did not significantly (p greater than 0.05) increase either the FcRs number on the PMNL surface or the phagocytic and bactericidal activity connected with these receptors. The possible mechanisms are discussed.
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PMID:Phagocytosis and intracellular killing of Staphylococcus aureus by bovine blood polymorphonuclear leukocytes after migration in vitro. 275 Mar 62

The ability of primed human polymorphonuclear leukocytes (PMNLs) to respond metabolically to stimulation with formylmethionyl-leucyl-phenylalanine (FMLP) was investigated. Cells isolated from an aseptic inflammatory reaction and from patients with a severe bacterial infection as well as cells that had been treated with a bacterial lipopolysaccharide were investigated. When these cells were compared to peripheral blood cells isolated from healthy controls, they were found to be metabolically primed, i.e., the cells gave rise to an increased chemiluminescence response to subsequent stimulation with the peptide. It was also shown that proportionally more of the activity generated from the primed PMNL was of an intracellular origin compared with that obtained from nonprimed cells. The biological effects induced by radicals produced extracellularly and intracellularly are discussed.
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PMID:Relationship between intracellularly and extracellularly generated oxygen metabolites from primed polymorphonuclear leukocytes differs from that obtained from nonprimed cells. 275 87

Sulfatide from the outer surface of Mycobacterium tuberculosis blocked priming in cultured human monocytes. Monocytes were primed in vitro with either lipopolysaccharide (LPS) or interferon-gamma. Primed monocytes released increased amounts of superoxide anion (O2-) when stimulated with formyl-methionyl-leucyl-phenylalanine or with phorbol myristate acetate. Primed monocytes also showed increased phagocytosis of sheep erythrocytes and increased release of interleukin 1. When primed monocytes were treated with 10 micrograms/ml of sulfatide, these enhanced functions, characteristic of primed monocytes, returned to levels found in unprimed monocytes. (With respect to these functions and others, monocytes or macrophages primed in vitro by exposure to LPS or interferon-gamma resemble macrophages activated in vivo by infection. In vivo, activated macrophages provide non-specific resistance to infection). Inhibition of priming by sulfatide could be detected within 10 min, but maximum effect of sulfatide required 3 to 5 hr. Sulfatide had no effect on O2- release, if it was added after the cells had been stimulated by PMA, suggesting that sulfatide did not inhibit enzymes involved in formation of O2-, but rather that sulfatide inhibited priming. Increasing the amounts of LPS or interferon-gamma did not counteract the effects of sulfatide. Sulfatide did cause monocytes to release some prostaglandin E2 (less than 1 nM), but the amount was not sufficient to inhibit monocyte functions. The effect of sulfatide was not blocked by indomethacin. Other sulfated compounds and other products of mycobacteria did not produce the sulfatide effect. We conclude that M. tuberculosis has on its outer surface a chemical that directly interferes with monocyte priming. In vivo, M. tuberculosis might use sulfatide to block macrophage activation and thereby resist being killed by macrophages.
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PMID:Inhibition of macrophage priming by sulfatide from Mycobacterium tuberculosis. 282 97

The release of superoxide (O2-) by polymorphonuclear leukocytes (PMN) is an important function that contributes to microbial death. Controversy exists as to the effect of bacterial endotoxin (lipopolysaccharide, or LPS) on the production of O2-. We have injected rabbits with 25 micrograms Escherichia coli LPS intravenously and studied PMN function 18 to 24 hours later. Relative to PMN from saline-injected controls, PMN from LPS-treated rabbits released markedly greater amounts of O2- in response to 10 ng/ml phorbol myristate acetate (PMA) as measured by nmol cytochrome C reduced in 20 minutes (40.8 +/- 7.8 for LPS-treated PMN versus 10.1 +/- 1.6 for control, p less than 0.01). LPS injection, however, significantly reduced O2- release in response to C (complement) 5a (1.4 +/- 0.6 nmole/20 minutes for LPS-treated PMN versus 5.6 +/- 1.3 nmole/20 minutes for control, p less than 0.01). O2- release in response to a third stimulus, n-formyl-methionyl-leucyl-phenylalanine (10(-7) to 10(-9) M), was not affected by LPS. O2- release in response to PMA was enhanced over a wide range of PMA concentrations (10 to 300 ng/ml). Kinetic studies over 30 minutes indicated that, after a brief initial latency in measurable response, LPS enhanced responsiveness to PMA at all time points observed. The reduced responsiveness to C5a corresponds to a previously reported down regulation of receptors for this ligand after intravenous LPS. The observations indicate that intravenous LPS can alter a critical function of PMN for at least 24 hours in a stimulus-specific manner.
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PMID:Stimulus-specific effects of endotoxin on superoxide production by rabbit polymorphonuclear leukocytes. 282 96


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