Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sera from normal healthy human adults and infants, as well as sera from mice, rabbits, and guinea pigs, were examined by immunoblotting for naturally occurring antibodies reacting with outer membrane proteins of two Escherichia coli strains, O111 and O18. Some individuals had antibodies reacting very strongly with the iron-regulated outer membrane proteins, including the ferric-enterochelin receptor protein (Mr, 81,000), as well as with ompA. However, sera from infants contained predominantly antibodies to ompA; antibodies recognizing the iron-regulated outer membrane proteins were either absent or barely detectable. In human serum the antibodies were mainly of the immunoglobulin G class. No serotype-specific antibodies to the lipopolysaccharide of E. coli O111 or O18 were found in the sera tested.
 ...
PMID:Naturally occurring antibodies in human sera that react with the iron-regulated outer membrane proteins of Escherichia coli. 298 39

Weanling male CD-1 mice were fed low-iron or iron-supplemented diets for 31 days. Mice fed the low-iron diet exhibited typical signs of iron deficiency, which included reduced weight gains (P = 0.0041) and anemia (P less than 0.0001). The effect of iron deficiency on antibody production, lymphocyte blastogenesis, and sensitivity to endotoxin were evaluated. Antibody production against sheep red blood cells, a T-lymphocyte dependent response, was reduced in iron-deficient mice (P = 0.0067). In contrast, antibody production against dinitrophenyl-ficoll, a T-lymphocyte-independent response, was not affected by iron deficiency (P = 0.291). Iron deficiency reduced T-lymphocyte blastogenesis induced by concanavalin A (P = 0.011), but had no effect on B-lymphocyte blastogenesis induced by Escherichia coli lipopolysaccharide (P = 0.662). These results indicate that the immunosuppressive effects of iron deficiency are related to T-lymphocyte function associated with lymphocyte proliferation and antibody production. A significantly increased susceptibility to endotoxin, a T-lymphocyte-independent response involving nonspecific defense mechanisms, was not observed in iron-deficient mice. Mortality associated with endotoxin was 14.2% in the iron-deficient mice as compared to 35% in the iron-replete mice (P = 0.079).
 ...
PMID:The effect of iron deficiency on the immune response in mice. 307 54

Atomic absorption spectroscopy of isolated native and EDTA-modified (lipopolysaccharide-depleted) outer membrane revealed trace amounts of potassium, manganese, and iron (1.0-7.0 nmol/mg dry weight outer membrane). Sodium, magnesium, and calcium were approximately one order of magnitude more plentiful, but EDTA-modified outer membrane was deficient in calcium. When metal-binding assays were conducted to find the binding capacity of native and EDTA-modified outer membrane, potassium bound poorly compared with sodium. However, there was no difference in the binding of these ions between the OM preparations. In contrast, reduced amounts of magnesium, calcium, manganese, and iron III bound to the EDTA-modified OM. Partitioning of intact cells in a biphasic dextran-polyethyleneglycol system indicated that the reduced lipopolysaccharide content of the EDTA-modified outer membrane increased the hydrophobicity of the cell surface. Exposure of control and EDTA-treated cells to divalent metal salt solutions before phase partitioning also increased cell surface hydrophobicity. Freeze-etching showed that sodium ions had no effect on the membrane fractures observed in control cells, but with EDTA-treated cells, this cation increased the occurrence of small outer membrane fractures (plateaus) which are characteristic of EDTA treatment. Both magnesium and manganese increased the frequency of outer membrane cleavage in control cells, whereas calcium did not. In contrast, all three divalent metallic ions increased the frequency and extent of cleavage in the outer membrane of EDTA-treated cells.
 ...
PMID:Physicochemical roles of soluble metal cations in the outer membrane of Escherichia coli K-12. 309 Dec 29

We tested several monokines and muramyl dipeptide (MDP) to determine whether they induce the L-arginine-dependent effector mechanism in cultured murine macrophages. Recombinant interferon-gamma (rIFN-gamma) and recombinant tumor necrosis factor (rTNF) synergize to induce nitrite (NO2-) and nitrate (NO3-) synthesis from L-arginine as well as to cause inhibition of the iron-dependent enzyme aconitase in macrophages. Unlike rTNF, recombinant interleukin 1 (rIL 1) and rIL 6/B cell stimulatory factor 2 (rIL 6/BSF-2) did not act as cofactors when added to macrophages in the presence of rIFN-gamma. rIFN-gamma plus MDP induced the L-arginine-dependent effector mechanism in murine macrophages. However, induction by rIFN-gamma plus MDP was inhibited by anti-rTNF antibodies which suppressed both NO2-/NO3- synthesis and aconitase inhibition. This result indicates that endogenously produced TNF is involved in the induction of the L-arginine-dependent effector mechanism when MDP is the co-stimulant with rIFN-gamma. In contrast, anti-rTNF antibodies did not fully suppress the effect of combining rIFN-gamma and lipopolysaccharide, suggesting that, in this case, activation of the L-arginine-dependent effector pathway may involve more than induction of TNF synthesis by the macrophages. These results provide information, at a biochemical level, on a mechanism through which combination of IFN-gamma and TNF can modulate macrophage functions involved in the control of cell proliferation.
 ...
PMID:Interferon-gamma and tumor necrosis factor induce the L-arginine-dependent cytotoxic effector mechanism in murine macrophages. 314 79

There is little information about the local and systemic antibody response to surface antigens of bacteria growing in situ in infected lesions in man. In this study, Pseudomonas aeruginosa was obtained directly from the infected wounds of two patients with burns and studied without subculture. Outer-membrane proteins (OMPs) were investigated and compared with those of cells cultivated in the laboratory, with the aim of selecting defined growth conditions to give surface antigens more closely resembling those found in vivo. Several high-mol. wt (77,000-101,000) proteins were expressed in the outer membranes of the bacteria from the patients and could be phenotypically induced by cultivating the same isolate in iron-depleted conditions in vitro. Other major OMPs (D, E, F, G and H) were also observed in cells taken from the lesions. Immunoblotting demonstrated that proteins D and E were recognised by different classes of immunoglobulins in the sera of both patients as was flagellar antigen present in the outer-membrane preparation of the P. aeruginosa from patient 1. Iron-regulated membrane proteins (IRMPs) were similarly detected, but more strongly by IgM from patient 1. Furthermore, a marked antibody response to IRMPs was noted at the site of infection. Bands of a similar intensity were seen after absorption of the sera with lipopolysaccharide (LPS) purified from the infecting strain. This indicated that the response observed was directed against OMPs (including IRMPs) and not against contaminating LPS.
 ...
PMID:Antibody response to outer-membrane antigens of Pseudomonas aeruginosa in human burn wound infection. 314 13

The systemic humoral immune response in cystic fibrosis (CF) to outer membrane (OM) proteins of Pseudomonas aeruginosa was investigated as a function of the time of colonization by immunoblotting. OM proteins were prepared from bacteria grown in ion-sufficient, magnesium-depleted, and iron-deficient media. The location of proteins F, H, and I on the blots was verified by monoclonal antibodies. Proteins H2 and H1 were differentiated by the overexpression of H1 under magnesium depletion. Iron-regulated membrane proteins (IRMPs) were recognized by their overproduction under iron limitation. Plasma samples from 43 CF patients and ten healthy adults were analyzed after preadsorption with lipopolysaccharide (LPS). Within the first year of colonization, only two to six specific plasma antibodies to OM proteins were produced. After a strong increase during the second year, long-lasting levels were seen in the majority of patients. Large variations of the immune response were noted among the patients. The number of specific antibodies to different OM proteins correlated with the severity of the course of lung disease. At maximum 38 immunostained bands were observed. Proteins H and I were the earliest antigens amongst the major OM proteins. During the second year, antibodies directed to protein F became detectable. IRMPs which indicate the growth of P. aeruginosa under iron deprivation were only recognized by plasma samples from chronically colonized CF patients with advanced lung disease.
 ...
PMID:Immune response in cystic fibrosis to outer membrane proteins of Pseudomonas aeruginosa. 314 71

Hybridoma-derived monoclonal antibodies were prepared against outer membrane antigens of four strains of Vibrio cholerae that were cultivated under iron-limited conditions, and these antibodies were partially characterized. We established a library of 66 hybridomas which produced monoclonal antibodies defining 16 different V. cholerae antigens. Two antigens (molecular weights, 18,000 and 112,000) were heat modifiable, whereas the reacting epitope of a third antigen (40,000-dalton-18,000-dalton doublet) was completely destroyed when it was heated at 100 degrees C. The 112,000-dalton heat-modifiable protein was an iron-regulated outer membrane protein. This protein bound 59Fe in vitro when it was combined with the V. cholerae siderophore-iron complex 59Fe-vibriobactin; it was also found in in vivo grown V. cholerae, as were three other antigens. A total of 26 hybridomas produced antibody to V. cholerae lipopolysaccharide. Of these, 12 were cross-reactive with lipopolysaccharides of other gram-negative bacteria, including 2 which recognized lipid A. Several of these anti-lipopolysaccharide monoclonal antibodies appeared to be lipopolysaccharide region specific. Some membrane antigens were strain specific, whereas others were common to both O group 1 and non-O group 1 vibrios.
 ...
PMID:Monoclonal antibodies to outer membrane antigens of Vibrio cholerae. 315 76

Many studies have shown that lactoferrin and transferrin have antimicrobial activity against gram-negative bacteria, but a mechanism of action has not been defined. We hypothesized that the iron-binding proteins could affect the gram-negative outer membrane in a manner similar to that of the chelator EDTA. The ability of lactoferrin and transferrin to release radiolabeled lipopolysaccharide (LPS) from a UDP-galactose epimerase-deficient Escherichia coli mutant and from wild-type Salmonella typhimurium strains was tested. Initial studies in barbital-acetate buffer showed that EDTA and lactoferrin cause significant release of LPS from all three strains. Further studies found that LPS release was blocked by iron saturation of lactoferrin, occurred between pH 6 and 7.5, was comparable for bacterial concentrations from 10(4) to 10(7) CFU/ml, and increased with increasing lactoferrin concentrations. Studies using Hanks balanced salt solution lacking calcium and magnesium showed that transferrin also could cause LPS release. Additionally, both lactoferrin and transferrin increased the antibacterial effect of a subinhibitory concentration of rifampin, a drug excluded by the bacterial outer membrane. This work demonstrates that these iron-binding proteins damage the gram-negative outer membrane and alter bacterial outer membrane permeability.
 ...
PMID:Damage of the outer membrane of enteric gram-negative bacteria by lactoferrin and transferrin. 316 87

Expression of alpha 1 proteinase inhibitor (alpha 1-PI) in human mononuclear phagocytes may provide a local mechanism for inactivation of serine proteases at sites of tissue injury, thereby preventing incidental damage to surrounding tissue and allowing for orderly initiation of repair. We have previously shown that serine (neutrophilic or pancreatic) elastase and lipopolysaccharide (LPS) each mediate an increase in the expression of alpha 1-PI in human peripheral blood monocytes and bronchoalveolar macrophages. In this study we demonstrate that elastase and LPS have an additive positive regulatory effect on alpha 1-PI expression. Distinct pretranslational and translational mechanisms of action for elastase and LPS, respectively, account for the additive effect. The possibility that translational regulation of alpha 1-PI by LPS involves a mechanism analogous to that of the yeast gene GCN4 during amino acid starvation and that of the human ferritin gene in response to iron is discussed.
 ...
PMID:Distinct and additive effects of elastase and endotoxin on expression of alpha 1 proteinase inhibitor in mononuclear phagocytes. 326 70

Fibrin formation in the kidney is frequently associated with clinically-significant renal dysfunction. We therefore measured and characterized the procoagulant activity (PCA) which is present in normal kidneys and in kidneys of rabbits with the Shwartzman phenomenon induced by two injections of bacterial lipopolysaccharide (LPS; E. coli LPS 055:B5,25 micrograms/kg and 50 micrograms/kg administered 24 hrs apart with rabbits sacrificed 12 hrs after the second injection). PCA was measured in sonicated tissue by one-stage coagulation assay. In normal kidneys the amounts of PCA in the inner medulla, outer medulla and inner cortex were 18.2 +/- 3.2, 44.1 +/- 3.8 and 78.5 +/- 5.7 percent, respectively, of that in the outer cortex (N = 31). Glomeruli (purified by the iron oxide magnetic method to greater than 95 percent homogeneity) contained 21.6 +/- 8.8 arbitrary units/micrograms protein compared with tubular fragments which contained 13.9 +/- 2.6 U/micrograms protein (N = 9). In LPS-treated rabbits PCA (in units/micrograms) increased in outer cortex from 33.7 +/- 3.9 (control) to 73.4 +/- 10.4 (LPS, P less than 0.01), in inner cortex from 26.7 +/- 2.9 (control) to 83.3 +/- 17 (LPS, P less than 0.02), in outer medulla from 12.9 +/- 2.4 (control) to 54.5 +/- 16.5 (LPS, P less than 0.05), and in inner medulla from 12.2 +/- 2.4 (control) to 32.1 +/- 4.9 (LPS, P less than 0.01). Glomerular PCA increased from 21.6 +/- 8.8 (control) to 88.8 +/- 20.7 (LPS) units/micrograms (P = 0.01), while tubular fragment preparation PCA increased from 13.9 +/- 2.6 (control) to 44.6 +/- 12.7 (LPS) U/micrograms (P = 0.02) (N = 9 per group).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Procoagulant activity in kidneys of normal and bacterial lipopolysaccharide-treated rabbits. 330 97


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>