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

Animals treated with formalinized Candida albicans manifest depressed cellular immune activity. Splenocytes from mice treated with as little as 14 micrograms of this material exhibited significantly reduced responses to the T cell-dependent mitogens phytohemagglutinin and concanavalin A. On the other hand, the B lymphocyte-dependent response to bacterial lipopolysaccharide was normal in these cultures. Splenocytes from treated mice were capable of actively suppressing the T cell- (but not B cell-) dependent proliferative response of normal cells. Analysis of splenocytes from Candida-treated mice showed that the suppressor cell is adherent to glass wool, is not adherent to Sephadex G-10, does not phagocytize carbonyl iron, is not susceptible to treatment with anti-Thy-1 plus C, but does bind specifically to anti-immunoglobulin- (anti-Ig) coated dishes. The adherence to the anti-Ig-coated dishes was not due to the simple attachment of Fc receptor-bearing lymphocytes, because dishes coated with the F(ab')2 fragment of rabbit antimouse IgG bound the suppressor cell. These results suggest that the active Candida-induced suppressor cell is composed, at least in part, of surface Ig-bearing B lymphocytes.
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PMID:Studies on the cellular nature of Candida albicans-induced suppression. 660 Jan 88

Iron-deficiency anemia impaired the blastogenic response of splenic lymphocytes and partially purified T cells to Concanavalin A and phytohemagglutinin. The response of splenic lymphocytes and partially B cells to bacterial lipopolysaccharide was also significantly impaired. Caloric restriction in pair-fed mice did not have any significant effect. Blastogenic response to the three mitogens was restored to normal after anemic mice were fed the regular diet containing 25 to 30 mg Fe/kg (FeSO4) for approximately 10 days. We also found that in the anemic mice the mean wet weights per 100 g of body of spleen, heart, brain, and kidney increased, while those of the thymus and liver decreased. In the pair-fed mice only the mean wet weight of the liver significantly decreased. There was a small but significant decrease in the white blood count and peripheral lymphocyte count in the anemic but not the pair-fed mice. The mechanism by which iron deficiency impairs the cell-mediated immune response is discussed.
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PMID:Impairment of blastogenic response of splenic lymphocytes from iron-deficient mice: in vivo repletion. 660 Mar 68

Splenic lymphocytes from iron deficient C57BL/6 mice gave smaller proliferative responses to T and B cell mitogens than those from either the control of pair-fed mice. The addition of hemin to the culture medium partially restored the responses to Con A and phytohemagglutinin but not to bacterial lipopolysaccharide in unfractionated spleen cells and enriched T cell fractions. The responses of lymphocytes from the control and pair-fed mice were either unchanged or decreased. Hemin restored the blastogenic response to Con A more efficiently than to phytohemagglutinin. The blastogenic responses were increased linearly with increasing doses of hemin. Ferric chloride and iron saturated mouse transferrin did not restore the response to either Con A or lipopolysaccharide. However, both transferrin and ferric chloride partially restored the response to phytohemagglutinin. The possible mechanism of selective restoration of blastogenesis by hemin, transferrin, and ferric chloride in iron-deficient T lymphocytes is discussed.
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PMID:Impairment of blastogenic response of splenic lymphocytes from iron-deficient mice. In vitro repletion by hemin, transferrin, and ferric chloride. 660 54

Intraperitoneal injection of Campylobacter fetus ss. jejuni into HAM/1CR mice was lethal, but viable counts of bacteria from whole body homogenates, organs and blood indicated that death was not due to sustained bacterial multiplication. Heat-killed organisms (5 X 10(9) cfu) injected into 7-day-old mice caused death within 24 h and this was shown to be due to endotoxin. Both ferric iron and heterologous lipopolysaccharide enhanced virulence; the LD50 was lowered from 1.8 X 10(9) cfu to 2.7 X 10(7) cfu when both were used. Three-day-old or adult animals survived challenge with Campylobacter fetus without clinical symptoms when challenged orally or by intravenous or intraperitoneal routes.
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PMID:Factors affecting the lethality of Campylobacter fetus subspecies jejuni in mice. 674 38

Previous work has shown that antibody and transferrin, acting together, exert a bacteriostatic effect on certain pathogenic Escherichia coli. This effect may be due to the ability of the antibody to interfere with the release of the iron chelator, enterochelin, from the bacterial cell. Enterochelin is essential for the transport of iron from transferrin to the bacterial cell. The nature of the bacterial antigen against which the antibody is directed has now been determined by means of adsorption experiments. It was found that absorption of serum either with hear-killed cells of E. coli O111 or with Boivin antigen abolished the bacteriostatic effect. A monosaccharide, which proved to be colitose (3,6-dideoxy-L-galactose), was isolated after acetic acid hydrolysis of the Boivin antigen. Colitose is the terminal monosaccharide of the O-specific side chain of the lipopolysaccharide from E. coli O111. This monosaccharide abolished the bacteriostatic effect of both whole serum and mixtures of antibody and iron-binding proteins. When administered by the intraperitoneal route, it reduced the resistance of mice to subsequent infection with E. coli O111. This ability of colitose to interfere with antibacterial mechanisms is in accord with published immunochemical studies.
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PMID:Bacteriostatic effect of serum: role of antibody to lipopolysaccharide. 699 11

Incorporation of [14C]-thymidine into mouse lymph node cells stimulated with either Con-canavalin A or lipopolysaccharide in serum-free medium was markedly enhanced by the addition of transferrin. Thymidine incorporation was similar in transferrin-containing serum-free medium and in medium containing 5% foetal calf serum. Transferrins from both homologous and heterologous species were equally effective, but iron-binding half-molecules of transferrin, and low molecular weight iron chelates produced no enhancement. The optimal response was obtained with 10--50 micrograms/ml of transferrin, and with 30%--70% iron saturation. Although the major function of transferrin in lymphocyte cultures is probably to supply iron, it may also fulfil other functions.
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PMID:The effect of iron and transferrin on the response of serum-free cultures of mouse lymphocytes to concanavalin A and lipopolysaccharide. 725 Oct 59

We studied the role of N-glycosylation of human lactoferrin (hLF) with respect to properties that are relevant to its antibacterial and anti-inflammatory activities. A human kidney-derived 293(S) cell line that constitutively expresses recombinant hLF (rhLF) was produced. The reactivity towards various antibodies of rhLF that had been expressed in the absence or presence of tunicamycin (which blocks N-linked glycosylation) did not differ from that of natural (human milk-derived) hLF. Cation-exchange chromatography and N-terminal protein sequencing showed identical cationic properties and an intact N-terminal sequence for rhLF and natural hLF. SDS/PAGE of rhLF expressed in the presence of tunicamycin revealed a protein with the same M(r) as that of enzymically deglycosylated natural hLF. Both glycosylated and unglycosylated rhLF appeared to be completely saturated with iron. The affinity of natural hLF, glycosylated and non-glycosylated rhLF for both human lysozyme (Kd 4.5 x 10(-8) M) and bacterial lipopolysaccharide did not differ. SDS/PAGE of hLF species subjected to trypsin indicated that unglycosylated rhLF was much more susceptible to degradation. Furthermore, this analysis suggests that N-glycosylation heterogeneity in natural hLF and rhLF resides in the C-lobe. Thus our results provide no argument for differential antibacterial and/or anti-inflammatory activity of natural and (glycosylated) rhLF and suggest that a major function of glycosylation in hLF is to protect it against proteolysis.
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PMID:Glycosylated and unglycosylated human lactoferrins both bind iron and show identical affinities towards human lysozyme and bacterial lipopolysaccharide, but differ in their susceptibilities towards tryptic proteolysis. 749 99

Biosynthesis of nitric oxide (NO) from L-arginine modulates activity of iron-dependent enzymes, including mitochondrial acontiase, an [Fe-S] protein. We examined the effect of NO on the activity of iron regulatory factor (IRF), a cytoplasmic protein which modulates both ferritin mRNA translation and transferrin receptor mRNA stability by binding to specific mRNA sequences called iron responsive elements (IREs). Murine macrophages were activated with interferon-gamma and lipopolysaccharide to induce NO synthase activity and cultured in the presence or absence of NG-substituted analogues of L-arginine which served as selective inhibitors of NO synthesis. Measurement of the nitrite concentration in the culture medium was taken as an index of NO production. Mitochondria-free cytosols were then prepared and aconitase activity as well as IRE binding activity and induction of IRE binding activity were correlated and depended on NO synthesis after IFN-gamma and/or LPS stimulation. Authentic NO gas as well as the NO-generating compound 3-morpholinosydnonimine (SIN-1) also conversely modulated aconitase and IRE binding activities of purified recombinant IRF. These results provide evidence that endogenously produced NO may modulate the post-transcriptional regulation of genes involved in iron homeostasis and support the hypothesis that the [Fe-S] cluster of IRF mediates iron-dependent regulation.
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PMID:Biosynthesis of nitric oxide activates iron regulatory factor in macrophages. 750 26

The effects of sub-MICs of ciprofloxacin and tobramycin on the cell surface characteristics and extracellular virulence factors of Pseudomonas cepacia were evaluated. Cells were grown in batch culture under iron-deficient and iron-replete conditions. At sub-MIC levels that did not affect bacterial growth cell surface hydrophobicity decreased under both iron-replete and iron-depleted conditions with ciprofloxacin, but increased with tobramycin under iron-sufficient conditions. Exopolysaccharide synthesis, lipase production and siderophore production were all significantly increased by the presence of ciprofloxacin under both growth conditions. Outer membrane protein and lipopolysaccharide profiles were not affected by exposure to the two antibiotics.
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PMID:Effect of sub-MIC antibiotics on the cell surface and extracellular virulence determinants of Pseudomonas cepacia. 751 77

Citrulline formation by Ca(2+)-calmodulin (CaM)-dependent nitric oxide synthase from bovine brain is inhibited reversibly by indazole, 5-nitro-, 6-nitro-, and 7-nitroindazole with IC50 values of 2.3 mM, 1.15 mM, 40 microM, and 2.5 microM, respectively. Inhibition of citrulline formation by 7-nitroindazole exhibited a Ki value of 0.16 microM and was competitive versus both arginine substrate and (6R)-5,6,7,8-tetrahydrobiopterin cofactor. The NADPH oxidase activity of bovine brain CaM-dependent nitric oxide synthase was inhibited by 7-nitroindazole with an IC50 value of 0.6 microM. Citrulline formation by the interferon-gamma/lipopolysaccharide-inducible nitric oxide synthase of murine macrophages (264.7 cell line) is inhibited reversibly by indazole, 5-nitro-, 6-nitro-, and 7-nitroindazole with IC50 values of 470, 240, 56, and 20 microM, respectively. Inhibition of citrulline formation by 7-nitroindazole exhibited a Ki value of 1.6 microM and was noncompetitive versus arginine substrate but competitive versus (6R)-5,6,7,8-tetrahydrobiopterin cofactor. None of the indazoles tested inhibited the cytochrome c reductase activity of either nitric oxide synthase isoform at concentrations up to 1000-fold higher than their IC50 values for inhibition of citrulline formation. These observations are consistent with the proposal that the indazoles exert their inhibitory actions by interaction with the heme-iron of nitric oxide synthase such that oxygen does not bind.
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PMID:The inhibition of the constitutive and inducible nitric oxide synthase isoforms by indazole agents. 751 13


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