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)

Standard preparations of immunoglobulin for intravenous use consist predominantly of IgG (greater than 95%). We have compared the ability of a standard preparation (Sandoglobulin) with that of a new preparation (Pentaglobin, containing 12% IgM and 12% IgA) to improve the opsonic activity of antibody-deficient human sera in vitro. Panhypogammaglobulinaemic sera were poorly opsonic for five of six organisms tested, particularly Pseudomonas aeruginosa, Escherichia coli and Streptococcus pneumoniae, but opsonized Staphylococcus aureus almost normally. Both immunoglobulin preparations significantly improved the opsonic activity of the antibody-deficient sera for most organisms. The major difference between the two preparations was the ability of Pentaglobin to supply opsonins for P. aeruginosa, E. coli and Klebsiella pneumoniae, while Sandogloblin was significantly more potent in opsonins for Haemophilus influenzae. Pentaglobin demonstrates significant in vitro opsonic activity, particularly for enterobacteria (coliforms) and P. aeruginosa. Its content of IgM antibodies appears to confer special properties on Pentaglobin not seen with standard preparations of immunoglobulin for intravenous use. Its place in clinical practice remains to be determined but it may have a possible role in augmenting host defence mechanisms in Gram-negative septicaemia.
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PMID:Opsonic activity of a new intravenous immunoglobulin preparation: Pentaglobin compared with sandoglobulin. 250 Feb 75

A case of diffuse panbronchiolitis (DPB), associated with benign monoclonal IgA gammopathy and IgA nephropathy is described. The IgA deposition in the glomeruli of the patient was identified as consisting mainly of the monoclonal IgA having the same idiotype as that of serum monoclonal IgA. Recurrent infections of Hemophilus influenzae and Pseudomonas aeruginosa in the respiratory tract might have enhanced IgA-mediated immunity at the mucosal surface of the bronchiole, and ultimately induced monoclonal IgA gammopathy and IgA nephropathy.
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PMID:A case of diffuse panbronchiolitis (DPB) with benign monoclonal IgA gammopathy and IgA nephropathy with monoclonal IgA deposition. 250 71

The interaction of human IgA antibodies with the classical pathway of complement activation was investigated in a homologous human system, by means of two IgA1 and three IgG1 myeloma proteins having antibody activity against a defined antigen, staphylococcal alpha-toxin. In a solid-phase antigen-dependent C3b-binding ELISA system, the monoclonal IgG antibodies were previously shown to activate the classical complement pathway synergistically, resembling polyclonal IgG antibodies, whereas IgA antibodies were unable to activate complement by either pathway. In the present study, IgA antibodies were found to inhibit significantly the activation of complement initiated by antigen-bound polyclonal or mixed monoclonal IgG antibodies, in relation to the amount of IgA antibodies applied and bound to antigen. IgA1 myeloma proteins devoid of antigen-binding activity were without effect. Inhibition was independent of the ability of the IgA antibodies to compete against the IgG antibodies in binding to antigen, and was demonstrable with physiological concentrations of antibodies. Similar results were obtained with polyclonal serum IgA having antigen-binding activity. However, the binding of C1q to antigen-complexed IgG was inhibited only by a monoclonal IgA antibody that could compete against one of the three monoclonal IgG antibodies that bound C1q synergistically. This observation implied that at least two mechanisms were involved in the inhibition of C3b fixation. Fab alpha fragments of monoclonal IgA antibodies, obtained by cleavage with IgA1 protease from Haemophilus influenzae type b, were found to have a similar inhibitory effect on C3b fixation to the intact IgA1 antibodies. This observation supports the hypothesis that IgA1 proteases contribute to the invasive pathogenicity of certain mucosal bacteria, by cleaving secretory IgA1 antibodies to antigen-binding Fab alpha fragments, which are not only defective in mucosal defense properties, but which also protect the organisms from other immune effector systems, such as complement activation.
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PMID:Anti-inflammatory activity of human IgA antibodies and their Fab alpha fragments: inhibition of IgG-mediated complement activation. 260 39

Fifty-one children between 22 and 158 months of age referred to an immunology clinic with a history of recurrent respiratory tract infections were prospectively evaluated for immunologic abnormalities. Ten of the subjects had a poor response to the Haemophilus influenzae type b (Hib) capsular polysaccharide vaccine (failure to mount a twofold increase in titer or achieve a postimmunization titer greater than 0.2 micrograms ab/ml). There were no differences in mean serum concentrations of IgG, IgM, IgA, isohemagglutinins, or anti-tetanus toxoid between the responders and the nonresponders. None of the 10 nonresponders were deficient in IgG2. Eight of the vaccine failures were immunized with an Hib conjugate vaccine (HbOC) consisting of Hib capsular oligosaccharides coupled to diphtheria toxin. All responded with at least a fivefold increase in antibody after primary immunization with HbOC. Seven of the eight had a postHbOC primary immunization titer greater than 1.0 microgram/ml. This study demonstrates that some children with recurrent infections and with normal IgG subclasses are unable to respond to Hib capsular polysaccharide. This defect, which can be circumvented by presenting the polysaccharide antigen in an alternative form, may be contributing to the symptomatology experienced by these patients.
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PMID:Selective antibody deficiency to Haemophilus influenzae type B capsular polysaccharide vaccination in children with recurrent respiratory tract infection. 262 Dec 46

IgA protease produced by various strains of Haemophilus influenzae can digest serum IgA and yield its fragments which can react with anti-IgA serum. We assayed IgA protease activity by detecting the digests of IgA by SDS-PAGE and immunoblotting. The digests were separated with SDS-PAGE, transferred to nitrocellulose membranes and detected with anti- (alpha chain of human IgA, its Fab and its Fc) immunoglobulin conjugated peroxidases. Using this method, we can determine which type of IgA protease is produced by various of H. influenzae strains. All the 20 strains isolated from respiratory tracts produced IgA protease.
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PMID:Detection of IgA protease from Haemophilus influenzae by immunoblotting. 267 Jun 4

Serum IgG contains 4 subclasses, IgG1 (60-66%), IgG2 (20-30%), IgG3 (less than or equal to 5%) and IgG4. Individual subclasses vary with respect to their physicochemical and biological properties. IgG subclass concentrations in serum are age dependent. IgG1 and IgG3 reach near to adult levels around the age of 3, IgG2 and IgG4 after the age of 6. Antibodies of certain specificities generally belong to a certain isotype (subclass) due to the isotype restriction. Patients with subclass deficiencies often suffer from recurrent infections. Those with IgG2 deficiency coften occurring with IgA and IgG4 deficiency) develop recurrent infection of the upper and lower respiratory tract often caused by pyogenic microorganisms (Haemophilus, Pneumo-(occus). Since early initiation of IVIG substitution therapy has a beneficial effect on long term prognosis the importance of early diagnosis is apparent.
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PMID:[Clinico-immunologic aspects of IgG subclass deficiency]. 268 36

Three generations of relatives of 58-year-old nonidentical twins with chronic bronchitis and fibrotic lung disease were evaluated. Sera of 23 family members, 14 with a history of excessive sinopulmonary infections, were examined for deficiencies of immunoglobulin classes, IgG subclasses, and specific antibody to tetanus toxoid and Hemophilus influenzae type b. Of 14 symptomatic family members, 12 had serum IgE concentrations less than 5 IU/ml. Four had values less than 1 IU/ml. Serum IgE was greater than 10 IU/ml in all nine asymptomatic individuals. Inheritance of low IgE appeared to be autosomal dominant, with variable penetrance. IgA was low normal (70-90 mg/dl) in three individuals. Two of these were IgE deficient. One symptomatic child had unmeasurable IgG2 (less than 10 mg/dl) and IgE (less than 0.5 IU/ml). This kindred demonstrates that IgE deficiency can be familial, and associated with sinopulmonary disease.
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PMID:Familial IgE deficiency associated with sinopulmonary disease. 276 11

Chronic experimental Haemophilus somnus pneumonia was produced in five 8- to 12-week-old calves to investigate host-parasite relationships in the respiratory tract. Calves were depressed and pyrexic and coughed intermittently for 3 days and then recovered except for sporadic coughing. Bacteria persisted in the lung for 6 to 10 weeks or more. Immunoglobulin G1 (IgG1), IgG2, and IgM but no IgA antibodies specific for H. somnus were detected in serum. Bronchoalveolar lavage samples contained detectable IgG1, IgG2, IgM, and IgA antibodies specific for H. somnus throughout most of the experiment. The kinetics of the isotypic antibody response against H. somnus in serum and bronchoalveolar lavage fluids differed, suggesting that both local and systemic antibody responses had occurred. Persistence of pulmonary infection for 10 weeks or more in the presence of antibody may be due to an inappropriate distribution of isotypes, toxicity of H. somnus for bovine macrophages, and perhaps other factors. Three of the calves were challenged with a 10-fold-higher dose of H. somnus at 10 weeks after the original inoculation. Immunity against H. somnus was indicated by the rapid clearance of bacteria from the lungs and the presence of minimal pneumonia at necropsy 3 days after bacterial challenge.
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PMID:Pulmonary persistence of Haemophilus somnus in the presence of specific antibody. 276 64

Host and bacterial factors were evaluated among 86 Minnesota children with Haemophilus influenzae type b disease detected by active surveillance after introduction of type b polysaccharide vaccine in the state. Children were 2-6 y of age. Thirty-three (38%) had been vaccinated. There was no significant difference between the frequency of low serum concentrations of IgM, IgA, IgG, or IgG2 in the vaccinated and nonvaccinated subjects (13% vs. 8%, P = .5). The presence of the Gm immunoglobulin allotype phenotype (1,3,17;23;5,13,21), previously associated with a lower relative risk of vaccine failure in children from other states, was associated with a fourfold decrease in the relative risk of vaccine failure in Minnesota (P less than .07). Haemophilus isolates from 58 of the children were available for clonal characterization by multilocus electrophoresis and outer membrane protein subtyping. There were no significant differences between the clone distribution of the strains causing disease in vaccinated and nonvaccinated patients, and nearly all disease-producing clones in Minnesota also are known to cause disease in other areas of the country. Thus, vaccine failure in Minnesota is infrequently associated with hypogammaglobulinemia or with infection by unusual clones of a H. influenzae type b. Also, the Gm phenotype associated with protection against vaccine failure in other areas of the USA appears to be protective in Minnesota.
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PMID:Host and bacterial factors associated with Haemophilus influenzae type b disease in Minnesota children vaccinated with type b polysaccharide vaccine. 278 47

Twenty children experienced 30 episodes of otitis media with effusion due to nontypeable (NT) Haemophilus influenzae in the first 2 years of life. The local and systemic immune responses to homologous strains of NT H. influenzae were determined by an immunodot assay. Strain-specific immunoglobulin G (IgG) antibody predominated in the middle ear fluid (MEF). It was detected in 91% of the children, compared with IgM in 48% (P less than 0.005), IgA in 52% (P less than 0.005), and secretory IgA in 18% (P less than 0.005). The titer (log2) of NT H. influenzae-specific IgG antibody (mean +/- standard error, 8.2 +/- 0.1) exceeded the titers of IgM (3.4 +/- 0.1), IgA (3.7 +/- 0.1), and secretory IgA (1.2 +/- 0.3). NT H. influenzae-specific antibody was detected exclusively in MEFs of individuals who possessed homologous serum antibody. Although antibody titers in MEF declined over time, serum antibody titers remained stable. These data suggest that immunity to NT H. influenzae in the middle ear, in part, reflects systemic immunity. Whereas local antibody disappears after resolution of the infection, systemic antibody persists.
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PMID:Otitis media in children: local immune response to nontypeable Haemophilus influenzae. 280 36


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