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)

Certain recombinant human cytokines have been shown to enhance polymorphonuclear leucocyte (PMN) responses to subsequent stimulation. Mononuclear cells (MNC) from normal healthy individuals were stimulated for 5 h with 1 micrograms/ml bacterial lipopolysaccharide (LPS) in order to induce production and secretion of inflammatory cytokines into the surrounding medium. These mononuclear cell conditioned media (MNCM) were then used to prime PMN isolated from healthy volunteers. Preincubating the PMN with MNCM for 15 min at 4 degrees C followed by washing and warming to 37 degrees C caused a 344% increase (n = 26) in the rate of superoxide anion production in response to zymosan-activated serum (ZAS), a source of C5a des arg. This effect could not be reproduced with recombinant human forms of interleukin 1 beta (Il-1 beta) or granulocyte-macrophage-colony stimulating factor (GM-CSF), although, with the latter, there was some effect when the preincubation stage was carried out for 60 min at 37 degrees C. Only recombinant human tumour necrosis factor-alpha (rh-TNF-alpha) gave a similar PMN priming effect to that seen with MNCM. This effect could not be reversed by washing away either the MNCM or rh-TNF-alpha. The priming effect could be markedly reduced (74.8%, n = 6) by employing the use of polyclonal antibody to TNF-alpha in the preincubation step; assaying for TNF-alpha in these MNCMs showed that the degree of priming corresponded to the amount of TNF-alpha present. Rh-TNF-alpha alone appeared to have very little direct stimulatory effect on respiratory burst activity. The results show that TNF-alpha produced by LPS stimulated MNC after 5 h binds to a PMN surface receptor in the cold and warming of the cells to 37 degrees C allows for an immediate and dramatic response to ZAS stimulation. This suggests that TNF-alpha is the important cytokine upregulating PMN responses to other physiological mediators, including C5a des arg during the early phases of an inflammatory reaction.
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PMID:The priming effects of the products of stimulated mononuclear cells on the response of neutrophils to C5a des arg. 200 16

Eleven species are actually recognized within the genus Yersinia of which three--Y. pestis, Y. pseudotuberculosis, and certain serovars of Y. enterocolitica--are important infectious organisms for humans and warm-blooded animals. The causative agents of yersiniosis, Y. pseudotuberculosis and Y. enterocolitica, occur world-wide in areas of moderate and subtropical climate. Asymptomatically infected warm-blooded animals, causing environmental contamination, are the most important factors for the epidemiology of yersiniosis; apathogenic Yersinia species and serovars, on the other hand, are largely adapted to environmental conditions and, with regard to their ecology, independent from warm- or cold-blooded host organisms. The agents are usually transmitted by the oral route with food-stuffs as the most important vehicle of human yersiniosis. For their isolation, enrichment procedures and selective media have been developed. The organisms are identified by biochemical reactions and can be differentiated by serological and, in case of Y. enterocolitica, also by phage-typing methods. The differentiation of pathogenic and apathogenic strains is of diagnostic importance and should be routinely performed; simple tests are available for this purpose. Demonstration of antibodies against cell-wall-associated (lipopolysaccharide) or plasmid-encoded (protein) antigens may confirm the diagnosis if the causative agents failed to be isolated.
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PMID:[Microbiology and epidemiology of Yersinia infections]. 207

Soluble interleukin 1 (IL 1) binding proteins were identified by gel filtration and covalent cross-linking of 125I IL 1 in normal human serum and inflammatory exudate. High molecular weight 125I IL 1 protein complexes occurred with both IL 1 alpha and IL 1 beta, however, high molecular weight binding appeared to be non-specific. One specific IL 1 beta binding protein was observed to elute at approximately 100 kDa on gel filtration when bound to 125I IL 1 beta. This complex migrated as a broad band at 60 kDa when covalently cross-linked and analyzed by SDS-PAGE. The protein did not bind 125I IL 1 alpha and 125I IL 1 beta binding was only displaceable by excess cold IL-1 beta. The production of the specific IL 1 beta binding protein was assessed in a number of cell populations. Unstimulated peripheral blood mononuclear cells (PBMNC) did not produce the binding protein, but stimulation with phytohemagglutinin (PHA) caused production within 24 hr and binding protein levels remained elevated for up to 7 days. Stimulation with lipopolysaccharide (LPS) and IL 1 alpha did not consistently induce synthesis of the binding protein. Ligand-binding studies were performed to compare solubilized EL 4 NOB.1 cell membrane IL 1 receptor (sIL 1R) with semi-purified IL 1 beta binding protein from pooled synovial fluid. The sIL 1R preparation bound ligand with an affinity of 168 pM while the IL 1 beta binding protein bound 125I IL 1 beta with an affinity of 370 pM. This protein may function as an important carrier molecule for IL 1 beta and determine its distribution and kinetics in vivo.
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PMID:A soluble binding protein specific for interleukin 1 beta is produced by activated mononuclear cells. 215 65

We studied the lipopolysaccharide (LPS) of Legionella pneumophila and six other Legionella species to determine whether strain differences were apparent. The LPS was purified by a cold ethanol extraction procedure, and total carbohydrates represented 10 to 20% of LPS weight. 2-keto-3-deoxyoctonate represented 1 to 13% of the total carbohydrate present in the LPS. By sodium dodecyl sulfate-polyacrylamide gel electrophoresis, all strains except L. dumoffi showed smooth-type LPS with multiple high-molecular-weight complexes. Proteinase K-treated, whole-cell lysates showed profiles similar to those of purified LPS. Each serogroup of L. pneumophila and each Legionella species had a distinct sodium dodecyl sulfate-polyacrylamide gel electrophoresis profile. L. pneumophila lipid A is antigenically related to the lipid A of Enterobacteriaceae. In immunoblot assays with the LPS of L. pneumophila serogroups 1 to 6 as antigens, serogroup-specific immune monkey sera recognized homologous purified LPS, but not the LPS of the five heterologous serogroups. These studies indicate that LPS composition may be a determinant of serogroup specificity as defined by the immunofluorescence-based serogrouping schema for L. pneumophila and other Legionella species.
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PMID:Serogroup specificity of Legionella pneumophila is related to lipopolysaccharide characteristics. 241 53

The antigen-independent binding of CD4+ T-lymphoblasts by alveolar and peritoneal macrophages and splenic dendritic cells (DC) was compared. DC formed clusters with T-lymphoblasts within 30 min at 37 degrees C, whereas alveolar and peritoneal macrophages did not. Antigen-independent binding developed between macrophages and CD4+ blasts by 4 h at 37 degrees C. Binding by alveolar macrophages was trypsin sensitive, magnesium dependent, serum independent, and cold insensitive, whereas binding by DC required serum and was inhibited by cold. Cluster formation (cell aggregates greater than 250 microns 2) by macrophages and CD4+ blasts was increased by interferon-gamma and phorbol esters, but diminished by lipopolysaccharide. However, each of these factors increased cluster formation by blasts with DC. Efforts to promote antigen-independent binding of T cells by Ia+ macrophages did not alter their poor accessory cell capacities. The role of cluster formation in accessory cell activities was examined. Inhibitors of DC clustering, including trypsin, paraformaldehyde, and tunicamycin, abrogated the ability of DC to support antigen presentation and lectin-mediated proliferation. It is concluded that rapid antigen-independent binding to T-cells is a distinct property that is restricted to DC. Exposure to LPS may down regulate nonproductive binding of T-cells to alveolar macrophages. Our data further suggest that accessory cell activities in the rat are not a function of alveolar macrophages and may be limited to specialized Ia+ cells of dendritic lineage.
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PMID:Antigen-independent binding of T-cells by dendritic cells and alveolar macrophages in the rat. 249 72

Previously we have demonstrated that eight out of nine IgG3 monoclonal antibodies (mAb) obtained from autoimmune MRL-lpr/lpr mice were able to self-associate and to precipitate in the cold (Gyotoku et al., J. Immunol. 1987. 138:3785). To determine whether the cryoprecipitation of IgG3 mAb is enhanced or inhibited in the presence of specific ligand, we have established eight IgG3 mAb reactive with 2,4-dinitrophenol (DNP) hapten: four mAb were obtained from fusion of spleen cells of C57BL/6 mice immunized with 2,4,6-trinitrophenylated keyhole limpet hemocyanin, three from 129/Sv and one from BALB/c immunized with DNP-lipopolysaccharide. Five of them induced cryoglobulins composed exclusively of the IgG3 mAb. The binding of negatively charged monomeric DNP-amino acid conjugates completely inhibited the cryoprecipitation of all the five cryoprecipitating anti-DNP IgG3 mAb, while the incubation with positively charged or neutral DNP-amino acid conjugates had variable effects: increase, inhibition or no change of the cryoprecipitation. In addition, positively charged DNP-amino acid conjugates were able to induce the cryoprecipitation of one of the non-cryoprecipitating anti-DNP IgG3 mAb. Our data showed that (a) IgG3 mAb derived from non-autoimmune strains of mice, similar to IgG3 mAb derived from an autoimmune MRL-lpr/lpr strain, possessed the unique property to self-associate and were able to form cryoglobulins in most cases; (b) although the Fc-Fc interactions of IgG3 mAb play a decisive role in IgG3 cold solubility, IgG3 cryoprecipitation was markedly influenced after interacting with their specific ligand, depending on the charge of the hapten-amino acid conjugate. This suggested that even minor interferences with the electrostatic equilibrium of the IgG3 by the binding of charged hapten molecules induced dramatic changes in the solubility of the IgG3 mAb at low temperature.
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PMID:Inhibition of cryoprecipitation of murine IgG3 anti-dinitrophenyl (DNP) monoclonal antibodies by anionic DNP-amino acid conjugates. 249 23

Myoglobin-specific, Iad-restricted cloned helper T cells and T hybridomas were found to directly kill Iad-bearing, myoglobin-pulsed B lymphoma targets and could also kill bystander targets, but only in the presence of antigen-pulsed antigen presenting cells (APC). The induction of the killing requires recognition of processed antigen in the context of class II major histocompatibility complex (MHC) molecules. Despite the specificity of induction, the bystander killing suggests a nonspecific lytic mechanism. The direct killing can be inhibited only by cold specific targets, whereas the bystander killing can be blocked by both specific and nonspecific targets. The cold target inhibition seems to be due to interference with effector-to-target contact or proximity rather than due to high-dose suppression of T-cell activation. Experiments using T-cell supernatants or cyclosporin A suggested that the helper T cells kill targets by synthesizing short-range soluble factor(s) with nonspecific killing activity de novo during the effector phase, but only while antigen-specific signal transduction is occurring. The mechanism of cold target inhibition appears to be absorption or consumption of a short-acting cytotoxic lymphokine by cells which must be able to interact closely with the effector cell. Normal spleen B cells, despite their capability for activating the helper T cells, cannot inhibit specific killing or be killed by helper T cells, even after lipopolysaccharide stimulation. Thus, although killing by helper T cells may play a negative feedback role in the normal immune response, our data raise the possibility that the helper T-cell-mediated killing may contribute to the immune surveillance against malignancy by virtue of the preferential killing of tumor cells either directly or indirectly.
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PMID:Cloned protein antigen-specific, Ia-restricted T cells with both helper and cytolytic activities: mechanisms of activation and killing. 295 81

To determine whether the reported absence of fever in full-term-pregnant ewes might be associated with shifts of regional blood flows from thermogenic tissues to placenta during this critical period, fevers were induced twice by injections of Escherichia coli lipopolysaccharide (LPS, 0.25 microgram/kg iv) into each of six Merino ewes from 8 to 1 days prepartum, and their regional blood flow distribution was measured with radioactive, 15-microns-diam microspheres before and during the rise in fever (when their rectal temperature had risen approximately 0.4 degree C). Unexpectedly, fever always developed, rising to heights not significantly different at any time before parturition [4-8 days prepartum = 0.81 +/- 0.23 degree C (SE); 1-3 days prepartum = 0.75 +/- 0.17 degree C) and similar to those in three wethers treated similarly (0.90 +/- 0.10 degree C). Generally, during rising fever, blood flow in the ewes shifted away from heat loss tissues (e.g., skin, nose) to heat production tissues (e.g., shivering muscle, fat) and cardiac output increased; blood flow through redistribution organs (e.g., splanchnic bed) decreased. The reverse occurred during defervescence. Utero-placental blood flow remained high in the febrile ewes. These regional blood flow distributions during febrigenesis and lysis are essentially the same as those during exposures to ambient cold and heat, respectively. Some differences in the responses of cardiac output and its redistribution, however, were apparent between wethers and pregnant ewes. We conclude that 1) the previously reported "absence of fever in the full-term-pregnant sheep" should not be regarded as a general phenomenon and 2) full-term-pregnant sheep support fever production without sacrificing placental blood flow.
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PMID:Fever and regional blood flows in wethers and parturient ewes. 340 61

When the core temperature stabilizes at a hyperthermic level after iv injection of lipopolysaccharide (LPS), the threshold core temperature for cutaneous vasoconstriction (Thcv) is significantly increased in hot and neutral environments, while the threshold core temperature for shivering (Thsh) is not significantly altered in hot or cold environments but is significantly reduced at thermoneutrality. This type of dissociated threshold alterations of thermoregulatory effector responses seems to be typical for the febrile response of rabbits to LPS. Because the same threshold dissociation can be demonstrated after icv injection of LPS, the systemic and the central effects of LPS in the generation of fever seem to be mediated by identical mechanisms. Prostaglandins of the E series (PGE), one of the mediators considered as important in fever generation, cause parallel increases in Thcv and Thsh when injected icv. This indicates that the mode of action of PGE on the central targets producing hyperthermia differs from that of the ensemble of mediators involved in the generation of LPS fever in rabbits. In rabbits pretreated with aspirin, the threshold dissociation after iv LPS injection still occurs. This indicates that factors other than PGE play an important role in the generation of the threshold dissociation of thermoregulatory effector responses, which is typical for LPS fever. These data indicate also that the states of activity of the thermoregulatory effectors involved in the febrile responses can be altered individually and that the activities of these effectors during LPS fever are quite different from their activities in the control state.
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PMID:Threshold dissociation of thermoregulatory effector responses in febrile rabbits. 347 79

Immune responses and hematologic alterations were investigated in splenectomized pigs after IM inoculation with Eperythrozoon suis. Early hematologic alterations were massive parasitism of RBC, severe hypoglycemia, moderate bilirubinemia, and mild anemia; later findings included severe anemia, minimal parasitism of RBC, spontaneous agglutination of RBC at 25 C and 4 C which was reversible at 37 C, transient thrombocytopenia, and mild bilirubinemia. The humoral immune responses consisting of a transitory hyperglobulinemia and increase of indirect hemagglutination (IHA) titers against E suis were attributed to immunoglobulin M cold agglutinins. Cell-mediated immune responses, measured by phytohemagglutinin- and pokeweed mitogen-induced lymphocyte blastogenesis, were reduced after massive parasitemia. Blastogenesis induced by Escherichia coli lipopolysaccharide mitogen was increased before the hyperglobulinemia and an increase in IHA titer. There was an increase in the uptake of [3H]thymidine by lymphocytes cultured without mitogens after the decline in total globulin concentration and IHA titer.
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PMID:Experimental porcine eperythrozoonosis: T-lymphocyte suppression and misdirected immune responses. 387 72


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