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

Sensitization of mouse splenic lymphocytes in vitro with sodium borohydride, suggesting that the biologic effects of sodium periodate are-treated autologous spleen cells stimulated a one-way mixed lymphocyte reaction and led to the generation of thymus-derived cytotoxic effector cells. These effectors were capable of lysing in 4 hr periodate-treated syngeneic and, to a lesser extent, periodate-treated allogeneic target cells. These results suggest that sensitization by periodate-treated autologous cells could result either from a specific reaction to modified self components or from a nonspecific mitogenic stimulation. Effector cells generated by allogeneic sensitization were detected on periodate-modified targets, irrespective of the H-2 antigens expressed by the targets. The effects of periodate modification on both stimulator and target cells were reversible by sodium periodate are dependent on the formation of a free aldehyde group on cell surface glycoproteins. Pretreatment of stimulator cells with neuroaminidase prevented the effect of periodate treatment, suggesting that the sensitization involves oxidized sialic acid residues. During the 4-hour 51Cr-release assay periodate-treated targets could be used to detect cytotoxic effector cells of any specificity. Fresh spleen cells and lymphocytes cultured for 5 days without antigen or in the presence of lipopolysaccharide did not lyse periodate-treated targets. An increasing level of cytotoxicity was detected on periodate-treated targets when the effector cells were generated, respectively, by stimulation with concanavalin A, by sensitization with periodate-modified autologous cells. Although the lysis of periodate-treated targets is itself nonspecific, effector cell specificity could be determined by selective blocking of the lytic phase with cells syngeneic to the stimulators. These results indicate that a nonspecific interaction can occur between lymphocytes and periodate-treated target cells, but that this interaction leads to lysis only when the lymphocytes were activated to become cytotoxic effectors.
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PMID:Effects of sodium periodate modification of lymphocytes on the sensitization and lytic phases of T cell-mediated lympholysis. 5 7

Bacterial O-antigens coupled to biotin were shown to function well as labelled antigens in direct enzyme immunoassay. O-polysaccharides released from lipopolysaccharides by mild acid hydrolysis were oxidized by sodium periodate at sites located within the lipopolysaccharide inner core region and the generated aldehyde groups were subjected to reductive amination with 1,3-diaminopropane to yield per-aminated O-polysaccharide derivatives. Biotin was coupled to the introduced amino groups by way of a N-hydroxy-succinimide ester derivative. Biotinylated polysaccharides were used in direct enzyme immunoassays, that employed monoclonal antibody coated microtitre plates and detection of bound biotinylated antigen by streptavidin/horseradish peroxidase reagent. The assay format was designed for rapid estimation of the affinity constants of monoclonal antibodies for small oligosaccharide inhibitors, but the assay is also well suited to fast and sensitive detection of bacterial O-polysaccharides at concentrations within the range 1-10 ng/ml.
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PMID:O-antigen biotin conjugates. Preparation and use in direct competitive enzyme immunoassays. 169 76

The presence of a chlamydia-specified antigen associated with the plasma membrane of infected cell lines was demonstrated by indirect immunofluorescence staining with a monoclonal antibody, designated 47A2, specific for the chlamydial genus-specific lipopolysaccharide (LPS) antigen. Staining of HeLa, L-929, and McCoy cells infected with the L2 or F serovar of Chlamydia trachomatis was observed either without fixation or following aldehyde fixation and brief drying. The 47A2-reactive antigen appeared to be present on the plasma membrane, on bleb-like structures on the host cell surface, and on proximal processes of neighboring uninfected cells. Antibodies to chlamydial protein antigens such as the major outer membrane protein produced no surface staining under similar conditions. Membrane vesicles elaborated from infected cells were enriched for the 47A2-reactive antigen. Superinfection of chlamydia-infected cells with vesicular stomatitis virus, an enveloped virus which buds from the plasma membrane, allowed purification of progeny virions that were enriched with chlamydial LPS. These results are consistent with the presence of chlamydial LPS in the plasma membranes of infected host cells.
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PMID:Accumulation of chlamydial lipopolysaccharide antigen in the plasma membranes of infected cells. 247 Jun 79

Conjugation of simple ketoses (such as 3-deoxy-D-manno-2-octulosonic acid and N-acetylneuraminic acid) and of various O-specific polysaccharides (from Aeromonas hydrophila and Aeromonas salmonicida) to the bifunctional spacer 1,6-hexanediamine, was achieved by reductive amination. The saccharide--1-(6-amino)-hexane alkyamines obtained were converted into the corresponding isothiocyanate derivatives and coupled to the free epsilon-amino group of lysine residues of the protein carrier bovine serum albumin. In similar manner, the aldehyde group introduced by selective periodate oxidation into the partially O-deacylated lipopolysaccharide of Vibrio anguillarum was conjugated to 1,6-hexanediamine, converted into the corresponding isothiocyanate and covalently attached to bovine serum albumin.
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PMID:Synthesis of glycoconjugates derived from various lipopolysaccharides of the Vibrionaceae family. 292 Jul 31

The structure of the polysaccharide chain of Shigella boydii type 2 lipopolysaccharide was established using mainly 13C-n.m.r. spectroscopy, partial hydrolysis, Smith degradation, and methylation analysis. The repeating unit of the polysaccharide was concluded to be a branched hexasaccharide, as follows: (formula in text). Acetaldehyde was detected in the hyrolysate of the lipopolysaccharide, but no evidence was obtained to indicate that acetaldehyde is located in the polysaccharide moiety.
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PMID:Somatic antigens of Shigella: the structure of the polysaccharide chain of Shigella boydii type 2 lipopolysaccharide. 636 79

Acid treatment of Pseudomonas aeruginosa immunotype 1 lipopolysaccharide generated a low-molecular-weight polysaccharide fraction that was detectable in agar gel immunodiffusion but did not induce antibodies or resistance to infection in mice. The polysaccharide was treated with periodate to generate additional aldehyde groups. Oxidized polysaccharide was covalently coupled by reductive amination to 1,4-diaminobutyl-derivatized bovine serum albumin. Physical properties of the conjugate were characterized by gel filtration and high-pressure liquid chromatography. The gelation activity of the conjugate in the Limulus amoebocyte lysate assay was 4,000-fold less than native lipopolysaccharide by weight. Mice immunized with the conjugate resisted challenge with P. aeruginosa immunotype 1 that killed 90% of mice immunized with saline. Immunization with the conjugate vaccine induced humoral immunoglobulin G that passively protected normal and burned mice. These results indicate that conjugation of nonimmunogenic polysaccharide antigen of P. aeruginosa restores immunogenicity similar to that of native lipopolysaccharide without restoring endotoxicity inherent in lipopolysaccharide.
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PMID:Preparation and characterization of a nontoxic polysaccharide-protein conjugate that induces active immunity and passively protective antibody against Pseudomonas aeruginosa immunotype 1 in mice. 642 46

The observation that spermine inhibits the endotoxin (lipopolysaccharide; LPS) induced production of nitric oxide (NO) in macrophages has been ascribed to the conversion of SP to active metabolites by the action of enzymes, such as diamine oxidases, found, for example, in bovine sera. Inhibitory effect is also observed with the oxidised metabolite of spermine, spermine dialdehyde (SDA). Inhibition appears to be at the level of induction of the inducible isoform of NO synthase (iNOS). Here we show that the activity of endogenous aldehyde dehydrogenase present in the cells influences the degree of inhibition seen with either spermine or SDA. Most significantly, inhibition of aldehyde dehydrogenase activity greatly increases (100 fold) the ability of spermine to inhibit the production of nitrite by LPS- induced macrophages. This is presumably by preserving aldehyde metabolites of spermine and thus increasing its action on the induction of iNOS. Thus, inhibition of aldehyde dehydrogenase activity in vitro or in vivo may be a useful approach to enhance the inhibitory effect of polyamines or polyamine aldehydes on iNOS induction.
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PMID:Inhibition of the induction of nitric oxide synthase by spermine is modulated by aldehyde dehydrogenase. 752 90

1. We have recently found that in the presence, but not in the absence, of foetal calf serum, spermine inhibits the production of nitric oxide (NO) in cultured J774.2 macrophages stimulated with bacterial endotoxin (lipopolysaccharide; LPS) or with gamma-interferon (IFN), showing that polyamines may act as suppressants of NO-mediated immune functions. Here, we have studied the mechanisms and the specificity of this inhibitory action. 2. Other polyamines, as well as spermine, inhibit the formation of NO in cultured J774.2 macrophages, with the order of potency being spermine > spermidine >> putrescine = cadaverine. This inhibition of NO formation is not due to any cytotoxic effect of these agents for they neither reduced mitochondrial respiration nor increased the release of lactate dehydrogenase into the supernatant. 3. Spermine is not a direct inhibitor of the activity of iNOS in induced J774.2 cells as measured by its lack of effect on the conversion of L-arginine to L-citrulline in homogenates. Neither spermine, nor its metabolites, interfere with the production of nitrite from NO or act as scavengers of NO. Thus, spermine is an inhibitor of the induction of iNOS. 4. Spermine inhibits nitrite formation in the presence of foetal, newborn or adult bovine serum, but not rat or human serum. 5. The effect of sper mine on nitrite production can be prevented by isoniazid, hydrazine or hydroxylamine, inhibitors of spermine oxidase, as well as by phenylhydrazine, an aldehyde inhibitor. We have, therefore, tested the effects of spermine dialdehyde or malon dialdehyde on the induction of iNOS. Spermine dialdehyde (SDA, 10(-5) M) inhibits nitrite formation by IFN-activated J774.2 cells in the absence of serum when given as a pretreatment but not when given 6 h after stimulation. In contrast, malon dialdehyde was ineffective. Thus, aldehyde metabolites of spermine, such as SDA, account for the inhibitory effect of polyamines on the induction of NOS in vitro. 6. The inhibitory effect of polyamines on iNOS induction appears to be fairly specific to iNOS, for spermine does not inhibit LPS-induced production of prostaglandin F2 alpha or tumour necrosis factor.
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PMID:The mechanism of the inhibitory effect of polyamines on the induction of nitric oxide synthase: role of aldehyde metabolites. 753 82

Ozone is a ubiquitous pollutant that can cause acute pulmonary inflammation, cellular injury and may contribute to the development or exacerbation of chronic lung diseases. Despite much research, the effects of ozone on humans and potential cellular mechanisms of injury are still uncertain. However, ozone has been reported to increase the formation of aldehydes that could react with cellular proteins. Therefore, the purpose of these studies was to determine whether 4-hydroxynonenal (HNE), a previously unidentified aldehyde product of ozone exposure, is formed in human subjects exposed to ozone, and whether the response of human alveolar macrophages (AM) following a 1-h exposure to 0.25 ppm ozone with moderate exercise could be mimicked by in vitro incubation of AM with HNE. Western analysis demonstrated increased HNE protein adducts in airway fluid and alveolar macrophages after ozone exposure. AM were examined for endotoxin (lipopolysaccharide [LPS])-stimulated interleukin-1 beta (IL-1 beta) release and expression of heat shock protein 72 (HSP72). Immediately after ozone exposure there was no change in HSP72, but a 5-fold increase occurred 4 h after exposure. By 18 h after exposure, HSP72 levels decreased to below comparable air-exposed levels. Immediately after ozone exposure there was no effect on IL-1 beta release stimulated by LPS. However, IL-1 beta release stimulated by LPS was significantly inhibited 4 h after ozone exposure. By 18 h after ozone exposure, IL-1 beta release stimulated by LPS returned to normal. Incubation of human AM in vitro with HNE induced HSP72 and blocked LPS-stimulated IL-1 beta release possibly by inhibiting interleukin converting enzyme. Consequently, the in vitro results and demonstration of HNE protein adducts following ozone exposure are consistent with HNE being involved in this process in vivo and suggest that the cellular toxic effects of ozone could be a result of thiol reactive aldehydes produced by ozone.
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PMID:4-Hydroxynonenal mimics ozone-induced modulation of macrophage function ex vivo. 870 85

Shigella, the etiological agent of bacillary dysentery, rapidly kills human monocyte-derived macrophages in vitro. Wild-type Shigella flexneri, but not a nonvirulent derivative, induced human macrophage apoptosis as determined by morphology and terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL). Shigella-mediated macrophage cell death was blocked by the peptide inhibitors of caspases, acetyl-Tyr-Val-Ala-Asp-aldehyde (acetyl-YVAD-CHO) and acetyl-Tyr-Val-Ala-Asp-chloromethylketone (acetyl-YVAD-CMK). Protection from apoptosis by YVAD was observed in monocytes matured in the presence or absence of colony-stimulating factors (CSF) like macrophage-CSF or granulocyte-macrophage-CSF. Furthermore, lipopolysaccharide (LPS) or gamma interferon (IFN-gamma) rendered human macrophages partially resistant to Shigella cytotoxicity. Macrophages stimulated with either LPS or IFN-gamma were also protected by YVAD from Shigella-induced cell death. During Shigella infections of human macrophages, interleukin-1beta (IL-1beta) was cleaved to the mature form. IL-1beta maturation was severely retarded by YVAD, indicating that IL-1beta-converting enzyme (ICE; caspase 1) is activated in Shigella-induced apoptosis. The finding that Shigella induces apoptosis in human macrophages by activating ICE supports the hypothesis that the acute inflammation characteristic of shigellosis is initially triggered by apoptotic macrophages which release mature IL-1beta during programmed cell death.
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PMID:The interleukin 1beta-converting enzyme, caspase 1, is activated during Shigella flexneri-induced apoptosis in human monocyte-derived macrophages. 939 11


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