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)

Major surface antigens of Bactmbrane complex by gentle methods, purified, and characterized immunochemically. A lipopolysaccharide (LPS) was found to be chemically distinct from the LPS of facultative gram-negative bacteria in that it lacked two core sugars, 2-keto-3-deoxyoctonate and heptose, as well as beta-hydroxymyristic acid, the predominant fatty acid in the lipid A moiety. The LPS was further atypical in that it had a very low level of biologic activity. A capsular polysaccharide was demonstrated morphologically by electron microscopy with ruthenium red staining and a ferritin-labeled antibody technique. This antigen was shown to be subspecies-specific by indirect immunofluorescence. Antibody to the capsular polysaccharide was measured by an enzyme-linked immunospecific assay. The presence of a relatively impotent LPS and a surface capsular antigen may partly explain the rarity of bacteremia and septic shock due to B. melaninogenicus subspecies asaccharolyticus and the common association of this organism with abscess formation.
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PMID:Immunochemical characterization of surface antigens of Bacteroides melaninogenicus. 4 22

Earlier studies, which indicated that high titers of O-specific antibody to the patient's infecting organism in acute-phase serum specimens were not associated with a decrease in the frequency of subsequent shock and death in bacteremia due to gram-negative bacilli, were reexamined for evaluation of the protective activity of specific IgG and IgM antibody. Titers of hemagglutination antibody and levels of IgM, determined by indirect immunofluorescent staining of the patient's infecting organism, as well as hemagglutination titers after reduction of serum with 2-mercaptoethanol and IgG levels, correlated closely (P less than 0.001). High titers of IgG antibody to the patient's infecting organism in acute-phase specimens were associated with a significant reduction in the frequency of shock and death in bacteremia. In contrast, high titers of IgG antibody were not associated with a diminution in the frequency of shock and death. The previously demonstrated protective activity of antibody to an antigen, Re lipopolysaccharide, shared by most gram-negative bacilli was reconfirmed and shown to be independent of the protective activity of O-specific IgG antibody.
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PMID:Effects of IgM and IgG antibody in patients with bacteremia due to gram-negative bacilli. 5 97

The involvement of multiple species and serologic types in gram-negative bacteremia prompted evaluation of immunization with shared, cross-reactive antigens of gram negative bacilli. Active and passive immunization with Re chemotype mutants of Salmonella minnesota afforded significant protection against heterologous gram-negative bacilli and were considerably more effective than immunization with smooth S. minnesota or its Ra, Rb, Rc, Rd1 and Rd2 mutants. Since the lipopolysaccharide of the Re mutant is composed solely of 2-keto-3-deoxycotonate (KDO) and lipid A, the protective activity of antibody to the Re mutant and lipid A was evaluated. Immunization with Re mutant protected granulocytopenic rabbits against lethal bacteremia and protected mice against lethal challenge with heterologous endotoxins, whereas antibody to lipid A had no protective activity. In concomitant clinical studies, high titers of antibody to the Re mutant at the onset of bacteremia were associated with a significant diminution in the frequency of shock and death, which was independent of any effect of O-specific antibody.
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PMID:Cross-reactive antigens: their potential for immunization-induced immunity to Gram-negative bacteria. 33 Jul 75

During a period of 13 months, 28 serious infections caused by Bacteroides were seen in 27 patients. Sixteen patients yielded Bacteroides fragilis; sera from 13 (81%) of these 16 had increased levels of IgG specific for B. fragilis lipopolysaccharide (LPS) antigens by enzyme-linked immunosorbent assay (ELISA). Sera from 20 normal controls did not have increased specific IgG. Sera from 22 of 23 patients with bacteremia caused by other gram-negative rods also failed to yield increased levels of specific antibody (P less than 0.0012). Analysis of sera from patients with B. fragilis infections disclosed a significant correlation between the levels of specific IgG to B. fragilis LPS measured by ELISA and the IgG antibody to the infecting B. fragilis by indirect immunofluorescence (r = 0.84, P less than 0.012). Two of the remaining 12 infections caused by Bacteroides not apparently due to B. fragilis organisms were also associated with increased levels of specific IgG to B. fragilis LPS antigens. Specific IgG antibody response may be an important adjunct in diagnosis of common B. fragilis infections and may allow better management of antimicrobial agents.
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PMID:Detection of specific IgG antibody in sera from patients infected with Bacteroides fragilis by enzyme-linked immunosorbent assay. 39 40

Serum antibodies to exotoxin A and type-specific lipopolysaccharide were measured by passive hemagglutination in 52 patients with Pseudomonas aeruginosa septicemia. Their comparative protective activities were evaluated by relating the titers of each at the onset of bacteremia to subsequent outcome. High acute serum antitoxin and antilipopolysaccharide titers (log2 reciprocal mean titers greater than 5) were associated with survival (76% of 17 with high vs. 46% of 24 with low antitoxin titers, P = 0.05; 85% of 13 with high vs. 48% of 29 with low antilipopolysaccharide titers, P = 0.03). In contrast, neither antibody titer was significantly associated (P less than or equal to 0.05) with patients' age or sex, severity of underlying disease, presence of leukopenia, steroid or immunosuppressive therapy. Despite a correlation between acute titers of the two antibodies (r = 0.33, P = 0.06), they appeared to protect independently and additively. Whereas 75% of 8 patients with high antitoxin titers and only 38% of 16 with low titers survived with low antilipopolysaccharide titers (P = 0.10), 100% (6/6), 73% (8/11), and 38% (6/16) survived, respectively, when both, one, or neither antibody was present in high titer (P = 0.01). Furthermore, the association between high acute serum antitoxin titers and survival was more pronounced in patients with rapidly fatal underlying disease (P = 0.06) and leukopenia (P = 0.12) than in more favorable prognostic and immune categories. These data indicate that serum antibodies to exotoxin A and lipopolysaccharide are found in most patients with P. aeruginosa septicemia and both are protective. Both antibodies may have therapeutic or prophylactic potential, whereas serum antiexotoxin A antibodies may be particularly beneficial in compromised hosts.
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PMID:Protective activity of antibodies to exotoxin A and lipopolysaccharide at the onset of Pseudomonas aeruginosa septicemia in man. 42 53

The protective efficacy afforded by immunization with the capsular antigen of Bacteroides fragilis against abscess formation and bacteremia due to this organism was studied in an experimental rat model of intraabdominal sepsis. Of unimmunized animals, animals immunized with methylated bovine serum albumin and complete Freund's adjuvant, and animals immunized with lipopolysaccharide of Bacteroides thetaiotaomicron, greater than 90% developed abscesses when challenged intraperitoneally with strains of B. fragilis or Bacteroides distasonis (given with an enterococcus) or with the cecal contents of meat-fed rats. In contrast, animals immunized with B. fragilis capsular polysaccharide, given with or without methylated bovine serum albumin and complete Freund's adjuvant, and animals immunized with the outer membrane of B. fragilis strain 23745 were protected to a significant degree from abscesses caused by challenge with B. fragilis or B. distasonis. Such immunization had no overall effect on the development of abscesses in animals challenged with the entire cecal contents of meat-fed rats; however, B. fragilis was eliminated from the abscesses of these animals. Animals immunized with the capsular polysaccharide were protected from early B. fragilis bacteremia.
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PMID:Protective efficacy of immunization with capsular antigen against experimental infection with Bacteroides fragilis. 52 89

Specific passive immunity against Pseudomonas aeruginosa sepsis was assessed in granulocytopenic dogs. Dogs were infused with either normal or antipseudomonas immune plasma 24 h before pseudomonas challenge. They were challenged intravenously with 10(7) serotype 6 P. aeruginosa during granulocytopenia. Treatment was evaluated by observation of survival periods, febrile responses, type 6 pseudomonas antibody titers, and quantitative cultures of blood and tissues. The results demonstrated that passively immunized dogs did not survive infection. Both normal-plasma and immune-plasma recipients had bacteremia at death, with median values of 980 and 470 pseudomonas per ml of blood, respectively. All dogs had marked febrile responses 24 h after pseudomonas challenge and had high concentrations of pseudomonas in their lung tissue at death, with median values of 10(8) pseudomonas per g of wet tissue weight. After plasma infusion, immune-plasma recipients had high concentrations of anti-pseudomonas antibody, with total antibody titers ranging from 256 to 1,024 and a median value of 1,024. These titers were comparable to titers attained in a previous study from our laboratory using active immunization with pseudomonas lipopolysaccharide vaccine, where the median total anti-pseudomonas antibody titer was 2,048. Actively immunized animals, however, were significantly protected against pseudomonas sepsis and had prolonged survival periods and prevention of bacteremia. The present study demonstrates that circulating type-specific antibody is not solely responsible for the protection afforded to granulocytopenic dogs actively immunized against pseudomonas.
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PMID:Passive immunity against pseudomonas sepsis during granulocytopenia. 82 5

Although Escherichia coli strains possessing the K1 capsule are predominant among isolates from neonatal E. coli meningitis and most of these K1 isolates are associated with a limited number of 0 lipopolysaccharide (LPS) types, the basis of this association of K1 and certain 0 antigens with neonatal E. coli meningitis is not clear. The present study examined in experimental E. coli bacteremia and meningitis in newborn and adult rats whether or not the K1 capsule and/or O-LPS antigen are critical determinants in the development of meningitis. Rats received subcutaneously at K1 E. coli strain (018+K1+) or mutants lacking either the K1 capsule (018+K1-) or 0 side-chain (018-K1+). 12-24 h later, blood and cerebrospinal fluid (CSF) specimens were obtained for quantitative cultures. The isolation of E. coli from CSF was observed in both newborn and adult rats infected with K1+ strains regardless of LPS phenotype (018+ or 18-) who also developed a high degree of bacteremia (e.g., greater than 10(4) CFU/ml of blood). In contrast, none of the newborn and adult rats infected with 018+K1- and developing bacteremia of greater than 10(4) were found to have positive CSF cultures. These findings indicate that the presence of the K1 capsule and a high degree of bacteremia are key determinants in the development of E. coli meningitis, suggesting that there may be specific binding sites present in the brain which have an affinity for the K1 capsule and thus may be responsible for the entry of K1-encapsulated E. coli into the meninges.
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PMID:The K1 capsule is the critical determinant in the development of Escherichia coli meningitis in the rat. 132

The fetus and newborn are particularly susceptible to Listeria monocytogenes infection. We used a newborn rat animal model to investigate neonatal host defense against Listeria. In this animal model, newborn (3-d-old) rats are more susceptible to L. monocytogenes than older animals. Juvenile (23-d-old) L. monocytogenes-infected rats pretreated with lipopolysaccharide (LPS) had a lower bacterial load in blood than control animals, whereas LPS pretreated newborn rats had a higher bacterial load. Because LPS is a potent inducer of tumor necrosis factor (TNF) and TNF enhances host defense against this organism in adult animals, we assessed TNF content in splenic homogenates for animals of different ages. The age at which TNF was detectable in L. monocytogenes-Infected rats corresponded to the age at which LPS became active in preventing severe bacteremia. TNF was less than 1 unit/mL in splenic homogenates taken from rats less than 8 d of age, whereas 16-d-old rats infected with L. monocytogenes 1 d earlier had greater than 80 units/mL (p less than 0.0001 for 3-d-old versus 16-d-old rats). We also assessed the responsiveness of rats to exogenous TNF-alpha. Juvenile rats pretreated with TNF-alpha before L. monocytogenes infection had decreased bacterial load in spleen (p less than 0.02 versus controls) and better survival at 7 d (p less than 0.05 versus controls), whereas newborn rats did not improve with TNF-alpha pretreatment (p greater than 0.05 treated versus controls for splenic bacterial load and 7-d survival).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of tumor necrosis factor-alpha and interferon-gamma in newborn host defense against Listeria monocytogenes infection. 143 1

Monoclonal antibody against human tumor necrosis factor alpha (TNF MAb) prevents death induced by intravenous gram-negative bacteria or lipopolysaccharide (LPS) in primates. Although these studies have demonstrated that TNF plays a prominent role in the development of lethal septic shock, exploration of dose-response relationships and possible mechanisms of protection have been limited. We addressed these questions in a series of experiments conducted in E. coli-challenged pigs. First, we determined that TNF MAb neutralized the cytotoxic activity found in septic pig plasma and in culture media from pig monocytes incubated with LPS. Second, we demonstrated that pretreatment with TNF MAb promotes survival, in a dose-dependent fashion, in an otherwise lethal E. coli bacteremic pig model. The results of the survival study highly correlate (r = 0.96, P < 0.01) the presence of TNF in the circulation with mortality. In an additional series of physiologic monitoring experiments designed to delineate possible mechanisms of protection, the authors demonstrate that TNF MAb pretreatment abrogates the prolonged leukopenia, thrombocytopenia, and microvascular leakiness resulting from intravenous bacterial challenge and maintains arterial blood pressure while diminishing pulmonary edema. These findings may provide a mechanism whereby neutralization of TNF systemically affords protection against the lethal sequelae of bacteremia.
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PMID:Efficacy of monoclonal antibody against human recombinant tumor necrosis factor in E. coli-challenged swine. 144 53


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