Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0348321 (Haemophilus)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The percentage of beta-lactamase producing Haemophilus influenzae strains from patients with meningitis in The Netherlands increased from 0% in 1975/1976 to 4.6% in 1985/1986 (n = 1559). Twenty-three isolates resistant to ampicillin, penicillin, chloramphenicol, rifampicin and/or tetracycline were subtyped to determine if one resistant strain was spreading. (Sub)typing was performed by capsular typing, analysis of the major outer membrane protein patterns on sodium dodecylsulfate gels (SDS-PAGE subtypes), lipopolysaccharide serotyping and biotyping. The (sub)types of the resistant strains were similar to those of sensitive strains, thus indicating that antibiotic resistant strains develop at random.
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PMID:Comparison of antibiotic resistant and sensitive strains of Haemophilus influenzae type b in The Netherlands by outer-membrane protein subtyping. 313 38

Haemophilus (Actinobacillus) pleuropneumoniae Serotypes 5 and 7 capsular antigens (CA-1) were precipitated from culture supernatants with N-cetyl-N,N,N,-trimethylammonium bromide (Cetavlon). CA-1 contained a carbohydrate to protein ratio of 2:1 for Serotype 5 and 3:1 for Serotype 7. Glucosamine and uronic acid were detected in CA-1 from both serotypes suggesting that the capsule contained hyaluronic acid. All mice immunized intraperitoneally with CA-1 vaccine were protected from death when challenged with 10X the LD50 of the homologous but not the heterologous serotype. Oil adjuvants and the use of young (6 h) cultures were necessary for CA-1 vaccines to be protective. Deproteinization of CA-1 with chloroform and butanol followed by pronase treatment resulted in failure to protect mice from death. The protective capsular protein antigen in CA-1 vaccine may not originate from the outer membrane (OM) since repeated washing of the OM to elute the capsular protein antigen rendered the OM vaccine completely nonprotective for mice. Vaccines prepared from cell-wall lipopolysaccharide also were nonprotective for mice. Passive immunization of mice with anti-CA-1 antibody produced in rabbits to Serotype 5 was highly protective (P less than 0.01) for mice when challenged with 10X the LD50 of the homologous serotype.
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PMID:Protection of mice against the lethal effect of an intraperitoneal infection with Haemophilus (Actinobacillus) pleuropneumoniae after vaccination with capsular proteins. 323 18

The serum antibodies against lipopolysaccharide of Hemophilus influenzae were measured in acute and convalescent phase sera from 30 patients with acute maxillary sinusitis using enzyme-linked immunosorbent assay. Levels of antibodies in the maxillary antral secretions were also measured. In convalescent phase sera from 15 patients with acute sinusitis due to H influenzae, there was a threefold, 1.5-fold, and threefold increase in the geometric mean titers of IgG, IgM, and IgA, respectively. In antral secretions, titers were significantly higher (p less than .01) in culture-positive patients than in culture-negative patients for all antibodies. These data indicate that the immune system has the ability to respond systemically and locally with specific antibodies against lipopolysaccharide of H influenzae.
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PMID:Immunologic responses against lipopolysaccharide of Hemophilus influenzae in patients with acute sinusitis. 325 88

Seven human monoclonal antibodies (HmAb) directed against outer membrane antigens of Haemophilus influenzae type b (Hib) were produced by fusing Sp2/HPT heteromyeloma cells with human tonsillar lymphocytes sensitized in vitro for 6 days. The heterohybridomas were maintained in culture for at least one year and secreted, when cultured in Dulbecco's modified Eagle's medium without fetal calf serum, between 1 and 15 micrograms/10(6) cells/ml/24 h. All of the HmAb were IgGs except HiH-12 which is an IgM. Antibodies directed against the lipopolysaccharide and proteins of apparent molecular masses of 43, 37 and 27 kDa were identified by immunoblotting of sodium dodecyl sulfate-polyacrylamide gel electrophoresis patterns of outer membrane. Binding radioimmunoassay with live bacteria showed that five out of seven HmAb adsorbed to cell surface-exposed antigenic determinants. HmAb HiH-6, HiH-7 and HiH-10 reacted with a surface-accessible determinant on the 43-kDa outer membrane protein. In a dot enzyme immunoassay, these HmAb recognized 103 out of 111 Hib strains isolated worldwide. The strains were selected to represent the most common genotypic variations among Hib. None of these HmAb reacted with other bacterial species tested. These HmAb may serve to study the bacterial surface antigens implicated in the human humoral response and protection to Hib infections.
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PMID:Heterohybridomas secreting human monoclonal antibodies against Haemophilus influenzae type b. 325 87

Murine macrophages of the P388D1 cell line stimulated with lipopolysaccharide (LPS) from Haemophilus actinomycetemcomitans Y4 released an interleukin-1 (IL-1) inhibitor, as well as IL-1. Maximal IL-1 activity in culture supernatants was detected after 24 h of culture. On the other hand, IL-1 inhibitor activity reached a maximum level after 72 h of culture. An IL-1 inhibitor was partially purified from the culture supernatant of P388D1 cells stimulated with Y4 LPS for 72 h by ammonium sulfate precipitation, followed by Sephacryl S-200 gel chromatography. A 160-kilodalton peak inhibitory to IL-1 and a 14-kilodalton peak showing IL-1 activity were separated by Sephacryl S-200 column chromatography. The partially purified IL-1 inhibitor significantly suppressed the proliferation of C3H/HeJ murine thymocytes that had been induced with murine and human IL-1 in the presence of a submitogenic dose of concanavalin A. The IL-1 inhibitor more strongly suppressed human recombinant IL-1 beta than human recombinant IL-1 alpha. This inhibitory activity of the partially purified preparation was unaffected by the presence of trypsin inhibitor and the protease inhibitor aprotinin. The IL-1 inhibitor did not exhibit either IL-2 or IL-2 inhibitor activity. The inhibitor suppressed C3H/HeJ thymocyte proliferation induced by IL-1 in the presence of a saturated concentration of IL-2 instead of a suboptimal concentration of concanavalin A. These results indicate that prolonged culture of Y4 LPS-stimulated murine macrophages releases a specific inhibitor of IL-1.
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PMID:Production of an interleukin-1 inhibitor by cell line P388D1 murine macrophages stimulated with Haemophilus actinomycetemcomitans lipopolysaccharide. 326 86

The factors responsible for blood-brain barrier (BBB) injury during bacterial meningitis are incompletely defined. We evaluated the role of Haemophilus influenzae type b (Hib) lipopolysaccharide (LPS) in the alteration of blood-brain barrier permeability (BBBP) in an adult, normal and leukopenic, rat model of meningitis. Intracisternal inoculation of Hib LPS resulted in (a) dose-dependent increases in BBBP from 2 pg to 20 ng, with significant attenuation in the peak response after challenge with 500 ng and 1 microgram; (b) time-dependent increases in BBBP, with a delayed onset of at least 2 h, maximum alteration at 4 h, and complete reversal at 18 h; (c) greater BBBP than after challenge with the live parent strain; (d) and a close correlation (r = 0.86) between CSF pleocytosis and BBBP at 4 h. The LPS effect was significantly inhibited by preincubation with Polymyxin B and neutrophil acyloxyacyl hydrolase, however two different oligosaccharide-specific monoclonal antibodies did not inhibit activity. No change in BBBP after inoculation with Hib LPS occurred in leukopenic rats. Hib LPS, in the setting of an intact leukocyte response, exerts profound effects on BBBP.
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PMID:Haemophilus influenzae lipopolysaccharide-induced blood brain barrier permeability during experimental meningitis in the rat. 326 27

The chemical structure of the lipopolysaccharide of a deep-rough mutant (strain I-69 Rd-/b+) of Haemophilus influenzae was investigated. The hydrophilic backbone of lipid A was shown to consist of a beta-(1',6)-linked D-glucosamine disaccharide with phosphate groups at C-1 of the reducing D-glucosamine and at C-4' of the non-reducing one. Four molecules of (R)-3-hydroxytetradecanoic acid were found directly linked to the lipid A backbone, two by amide and two by ester linkage (positions 2,2' and 3,3', respectively). Laser-desorption mass spectrometry showed that both 3-hydroxytetradecanoic acids linked to the non-reducing glucosamine carry tetradecanoic acid at their 3-hydroxyl group, so that altogether six molecules of fatty acid are present in lipid A. The lipopolysaccharide was the first described to contain only one sugar unit linked to lipid A. This, sugar in accordance with a previous report [Zamze et al. (1987) Biochem. J. 245, 583-587], was shown to be a dOclA phosphate. The phosphate group was found at position 4, but the analytical procedures employed (permethylation and methanolysis followed by gas-liquid chromatography/mass spectrometry) also revealed dOclA 5-phosphate. Since a cyclic 4,5-phosphate could be ruled out by 31P-NMR, we conclude that, in this lipopolysaccharide, a mixture of dOclA 4- and 5-phosphate is present. By methylation analysis of the dephosphorylated, deacylated and reduced lipopolysaccharide the attachment site of the dOclA was assigned to position C-6' of the non-reducing glucosamine of lipid A. The anomeric linkages present in the lipopolysaccharide were assessed by 1H-NMR and 13C-NMR of deacylated lipopolysaccharide. The saccharide backbone of this Haemophilus influenzae lipopolysaccharide possesses the following structure: (Formula; see text)
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PMID:Chemical structure of the lipopolysaccharide of Haemophilus influenzae strain I-69 Rd-/b+. Description of a novel deep-rough chemotype. 326 41

In the course of using the infant rat model to determine the ability of various rabbit antisera to protect against challenge by Haemophilus influenzae type b we made two unexpected observations. In these experiments 4-day-old rats were inoculated s.c. on the dorsum with either rabbit serum or physiological buffers (sham serum) and then were challenged the next day with H. influenzae type b injected i.p. Bacteremia, as a marker for disease, was measured 24 h later on day 6. We observed the following. (i) Pre-immune, i.e., normal rabbit serum, containing minimal levels of antibodies to outer membrane proteins and depleted of antibodies to capsule and lipopolysaccharide, nevertheless significantly (P less than 0.01) protected the rats from challenge with H. influenzae type b when compared to a sham inoculation of buffer; (ii) In the absence of a serum inoculation on day 4 (a buffer was used as a sham serum inoculation), the levels of bacteremia obtained after inoculation with bacteria on day 5 depended upon the composition of the buffer in which the H. influenzae inoculum was suspended. Use of phosphate buffered saline (PBS) resulted in higher levels of bacteremia than PBS containing 0.5% bovine serum albumin (PBS-BSA) (P less than 0.001), i.e. the BSA apparently acted to protect the rats from H. influenzae infection. In fact the use of PBS-BSA as an inoculum buffer masked the protective effect noted above of the absorbed normal rabbit serum.
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PMID:Unexpected effects of absorbed normal rabbit serum and bovine serum albumin on survival of Haemophilus influenzae type b in the infant rat. 326 78

Ribosomal preparations from Klebsiella pneumoniae, Haemophilus influenzae, Streptococcus pyogenes, and Streptococcus pneumoniae were investigated with respect to their activating capacity towards murine lymphoid cells. The proliferation of BALB/c spleen cells was induced in a dose-dependent fashion (from 1 to 100 micrograms/ml) by ribosomes of K. pneumoniae, H. influenzae, and S. pyogenes with a peak activity at 48 or 72 hr of culture. The majority of the blast cells induced by these ribosomal preparations were positive for surface-immunoglobulin (S-Ig) and negative for Thy 1.2. Furthermore, K. pneumoniae, H. influenzae, and S. pyogenes ribosomes induced the synthesis of IgM and some IgA. Cell proliferation and induction of IgM production were also demonstrated with the 3 ribosomal preparations using spleen cells from athymic nude (nu+/nu+) mice, Lyb-5-defective CBA/N spleen cells, B cell-enriched and T cell-depleted BALB/c spleen cell suspensions, as well as spleen cells from the Ips gene-deficient C3H/HeJ strain. Cell culture supernatants contained specific anti-ribosome IgM antibodies. Antibodies of other specificities (anti-sheep erythrocytes) were also demonstrated in supernatants from K. pneumoniae-stimulated cultures. Evidence against a possible role of contamination of K. pneumoniae and H. influenzae ribosomes by lipopolysaccharide- or lipid A-associated proteins in this effect is discussed. Ribosomes from S. pneumoniae did not induce 3H-thymidine incorporation nor Ig production. None of the 4 ribosomal preparations was found to stimulate T cell blastogenesis or to induce interleukin-2 production by naive BALB/c spleen cells. Finally, ribosomes from H. influenzae, S. pyogenes, S. pneumoniae but not those of K. pneumoniae stimulated interleukin-1 production by adherent spleen cells, from BALB/c mice.
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PMID:Induction of murine B cell proliferation and immunoglobulin synthesis by some bacterial ribosomes. 326 81

Purified lipopolysaccharide (LPS) from Haemophilus influenzae type b (Hib) was examined for its capacity to interact with human hemolytic complement, generate conversion products of C3, C4, and factor B, stimulate C5a activity, and affect human neutrophil chemiluminescence and phagocytosis. Salmonella typhimurium LPS and Salmonella minnesota Rb LPS (R345 mutant) were examined for comparison. Incubation of Hib LPS with human serum deficient in gamma-globulin or with normal human serum containing 10 mM EGTA and 7 mM MgCl2 resulted in some depletion of hemolytic complement and conversion of C3 to degradation products (determined by inhibition of passive hemolysis and electrophoresis/immunofixation, respectively), indicating that complement activation occurred by the alternative pathway. Complement activation by Hib LPS and S. minnesota Rb LPS was similar, but significantly less effective than by S. typhimurium LPS (p less than 0.01). Solubilized Hib lipid A, but not LPS, induced conversion products of C4 in hypogammaglobulinemic serum, indicating activation of the classical pathway. Similar levels of C5a activity were generated by incubation of Hib LPS and S. typhimurium LPS in hypogammaglobulinemic serum, as determined by neutrophil shape change and neutrophil aggregation. Hib LPS directly stimulated neutrophil chemiluminescence, whereas S. typhimurium LPS had little effect. Phagocytosis of radiolabeled, opsonized Hib by neutrophils was diminished by S. minnesota Rb LPS, Hib LPS, or solubilized Hib lipid A (p less than 0.001), but was slightly increased by S. typhimurium LPS. Neither the oligosaccharide of Hib LPS or Hib capsular polysaccharide was capable of interacting with complement or altering neutrophil chemiluminescence or phagocytosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of Haemophilus influenzae type b lipopolysaccharide on complement activation and polymorphonuclear leukocyte function. 332 33


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