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)

Specific IgG and IgA antibodies against the outer membrane proteins of non-typable Hemophilus influenzae were investigated in otitis media with effusion in children. Amounts of these antibodies were determined in middle ear effusions (MEEs) and in sera by enzyme-linked immunosorbent assay. At the same time the amounts of total IgG and IgA antibodies in MEEs in comparison with those in sera were analyzed by laser nephelometry. The amounts of specific and total IgG and IgA in the MEEs were higher than those in the sera. The MEEs/sera ratios of IgG and IgA antibodies in the children with mucoid effusions were higher than those in the children with serous effusions. The exception involved IgG determined by laser nephelometry. These data support the hypothesis that bacterial infections and the subsequent immune response contribute to the prolongation of otitis media with effusion in children, especially when effusions become mucoid.
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PMID:The immunological role of the outer membrane proteins of non-typable Hemophilus influenzae in otitis media with effusion in children. 176 12

Immunoglobulin (Ig)A proteases synthesized by human mucosal pathogens have a unique specificity for human IgA and will not cleave IgA from other species. In contrast, animal pathogens have not reliably been shown to cleave IgA of the animals they infect. This lack of an animal model has prevented an understanding of the importance of IgA1 proteases as virulence factors. One strategy to develop an animal model would be to identify a species capable of infection by a human IgA-producing pathogen whose IgA was susceptible to cleavage by IgA1 protease of that bacterium. The chimpanzee can be infected with Haemophilus influenzae and is closely related immunologically to man. For these reasons it was sought to determine whether chimpanzee secretory IgA (SIgA) is susceptible to cleavage by IgA1 protease of H. influenzae. This report shows that chimpanzee SIgA can indeed be cleaved at the hinge region by H. influenzae IgA1 protease into Fab alpha and (Fc alpha)2.SC fragments. The susceptibility of chimpanzee SIgA to IgA1 protease of a human pathogen could serve as the basis of an animal model to determine the importance of IgA1 protease in pathogenesis.
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PMID:Cleavage of chimpanzee secretory immunoglobulin A by Haemophilus influenzae IgA1 protease. 179 27

Levels of salivary antibodies directed against Haemophilus influenzae b (Hib) capsule, measured by ELISA and standardized to the total salivary IgA, were compared among 57 patients with Hib infections, 117 household and 49 day care contacts of patients, and 53 control individuals with no known contact with Hib. Nineteen of the household or day care contacts were throat or nasopharyngeal culture positive for Hib. Eighty % of evaluable patients had polyribosylribitol phosphate (PRP)-specific IgA in their saliva, compared with 36% of contacts who were throat or nasopharyngeal culture positive for Hib, 53% of contacts who were throat or nasopharyngeal culture negative for Hib, and 30% of control children. In patients, no correlation between age and level of salivary anti-PRP antibody was seen, but patients less than 3 y old were more likely to have these antibodies than were older patients. Salivary PRP-specific IgA antibodies, associated with either Hib colonization or PRP vaccination, tended to decline over time. Thus, PRP-specific IgA antibodies can be identified in the saliva of children over a wide age range, including those colonized with Hib or vaccinated with PRP, but these antibodies appear to decline after antigenic stimulation ceases.
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PMID:Mucosal antibodies to Haemophilus influenzae type b capsular polysaccharide. 189 45

The occurrence of IgG, IgM and IgA class antibodies against a type-specific capsular polysaccharide of Streptococcus pneumoniae (Pn) and against a whole cell antigen of Haemophilus influenzae (Hi) and Branhamella catarrhalis (Br) was studied using the ELISA method on middle ear effusion (MEE) samples of 85 patients and paired serum samples of 40 patients during the course of acute otitis media (AOM). Although specific antibodies to all of these three bacteria appeared in MEE during the course of an AOM episode, antibodies against the infecting bacteria of that particular AOM episode were more often prominent. The antibodies were also detectable in the MEE without simultaneous presence in the serum. The middle ear infection was prolonged more often if specific antibodies to the infecting bacterium could not be detected in the MEE obtained at the beginning of the AOM attack. The present study indicates that AOM caused by Pn, Hi or Br may induce both a systemic and a local production of specific antibodies against the causative organisms during the course of otitis media. The occurrence of such antibodies in MEE seems to play a major role in the resolution of AOM.
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PMID:Occurrences of antibodies against Streptococcus pneumoniae, Haemophilus influenzae and Branhamella catarrhalis in middle ear effusion and serum during the course of acute otitis media. 190 85

The amino acid sequence T-P-P-T-P-S-P-S is tandemly duplicated in the heavy chain of human immunoglobulin A1 (IgA1), the major antibody in secretions. The bacterial pathogen Streptococcus sanguis, a precursor to dental caries and a cause of bacterial endocarditis, yields IgA protease that cleaves only the Pro-Thr peptide bond in the left duplication, while the type 2 IgA proteases of the genital pathogen Neisseria gonorrhoeae and the respiratory pathogen Haemophilus influenzae cleave only the P-T bond in the right half. We have sequenced the entire S. sanguis iga gene cloned into Escherichia coli. A segment consisting of 20 amino acids tandemly repeated 10 times, of unknown function, occurs near the amino-terminal end of the enzyme encoded in E. coli. Identification of a predicted zinc-binding region in the S. sanguis enzyme and the demonstration that mutations in this region result in production of a catalytically inactive protein support the idea that the enzyme is a metalloprotease. The N. gonorrhoeae and H. influenzae enzymes were earlier shown to be serine-type proteases, while the Bacteroides melaninogenicus IgA protease was shown to be a cysteine-type enzyme. The streptococcal IgA protease amino acid sequence has no significant homology with either of the two previously determined IgA protease sequences, that of type 2 N. gonorrhoeae and type 1 H. influenzae. The differences in both structure and mechanism among these functionally analogous enzymes underscore their role in the infectious process and offer some prospect of therapeutic intervention.
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PMID:Analysis of the immunoglobulin A protease gene of Streptococcus sanguis. 198 65

The safety and immunogenicity of Haemophilus influenzae type b-tetanus toxoid conjugate vaccine (Hib-TT) were evaluated in 77 healthy infants receiving injections at 3, 5, 7, and 18 months of age. No serious local or systemic reactions were noted. After the first injection the geometric mean Hib antibody level rose to 0.55 micrograms/ml, and each subsequent injection elicited a statistically significant rise in the geometric mean. The percentage of vaccinees with Hib antibody levels greater than 0.15 micrograms/ml serum was 75.5% after the first, 97.4% after the second, and 100% after the third Hib-TT injection. This percentage fell to 90.9% at 18 months of age but rose again to 100% after the fourth injection. Control infants (n = 10) injected with diphtheria-tetanus toxoid-pertussis vaccine only had nondetectable levels after the second injection. Hib-TT elicited increases of Hib antibody in all isotypes: IgG greater than IgM greater than IgA. Among IgG subclasses the highest increases were of IgG1. All vaccinated subjects had greater than 0.01 U/ml of TT antibody (estimated protective level) throughout the study. We conclude that Hib-TT, injected at 3, 5, 7, and 18 months, is safe and induces protective levels of antibodies during the age of highest incidence of meningitis caused by Hib.
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PMID:Clinical and immunologic responses to Haemophilus influenzae type b-tetanus toxoid conjugate vaccine in infants injected at 3, 5, 7, and 18 months of age. 199 43

To characterize the middle and inner ear cellular inflammatory responses to otitis media using immunohistochemical methods, we inoculated type B Haemophilus influenzae into the middle ears of healthy adult BALB/c mice. Mac-1+ neutrophils and macrophages appeared in the middle ear at 3 days. Lyt-1+ T cells and Lyt-2+ T suppressor/cytotoxic cells entered the middle ear mucosa on days 7 and 14. IgG+ and IgM+ T cells were present at all time points, with IgA+ lymphocytes forming the majority of mucosal immunoglobulin-bearing cells at 2 weeks. The cochlear scala tympani contained Lyt-1+ and Mac-1+ cells and two endolymphatic sacs stained diffusely with anti-IgA and -IgG antibodies. Lyt-1/L3T4+ T lymphocytes greatly outnumbered B lymphocytes, suggesting that helper/inducer T cells play a more important role in acute otitis media than has been recognized. Inner ear changes occurred after a single episode of otitis media.
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PMID:Type B Haemophilus influenzae-induced otitis media in the mouse. 204 46

Primary B-cell immunodeficiency is relatively frequent and may result in recurrent bacterial infections involving notably the respiratory tract, and in chronic severe enteroviral infections in patients with agammaglobulinaemia. Selective IgG2 isotype deficiency results in pneumococcal, Haemophilus influenzae and pseudomonal infections, since it is associated with defective production of antibodies that are specifically directed against bacterial capsular polysaccharides. Progress has recently been achieved in the determination of genetic and molecular bases of some of these immunodeficiencies. In X-linked agammaglobulinaemia, the abnormal gene has been located on the long arm of the X chromosome (Xq22-23); the intrinsic B-cell abnormality blocks differentiation at the pre-B stage, before the genes coding for light chain immunoglobulins are rearranged. There is now a strong suspicion that IgA deficiency, hypoglobulinaemia with variable expression and some selective IgG isotype deficiencies are three ways of expressing one single abnormality a genetic factor of which is located in the class III region of the HLA complex and perhaps also associated with HLA class II DQ. Treatment of deficient IgG production with intravenous immunoglobulin has thoroughly altered the prognosis of these diseases. Complete IgA deficiency carries a risk of accident by production of anti-IgA antibodies, which means that patients with isolated IgA deficiency should not be treated, that these antibodies should systematically be looked for in patients with IgA deficiency associated with partial deficiency of other immunoglobulins, and that these patients should be treated with IgA-free immunoglobulin preparations.
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PMID:[Primary immune deficiencies of B-lymphocytes]. 204 14

The role of secretory immunoglobulin (Ig) A in nasopharyngeal secretions in the adherence of Streptococcus pneumoniae and Hemophilus influenzae to nasopharyngeal epithelial cells was investigated in vitro. The adherence was remarkably reduced by treating bacteria with nasopharyngeal secretions, and the antiadhesive activity was significantly greater in nasopharyngeal secretions having secretory IgA antibody activity against bacteria than in those having no activity. Noticeable changes were not observed in the antiadhesive activity caused by absorption of IgG from nasopharyngeal secretions. Results suggest that secretory IgA in nasopharyngeal secretions is related to bacterial adherence and adds to the prevention of nasopharyngeal infections.
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PMID:Inhibition of bacterial adherence by nasopharyngeal secretions. 205 85

An association between humoral immune deficiency and childhood autoimmune disease has been previously established. We describe a 7-year-old male with severe autoimmune disease, recurrent infections, a marked deficiency of IgG2 and IgG4, and an inability to respond to polysaccharide antigens. This child was also found to have isolated growth hormone (GH) deficiency. Laboratory results included a positive anti-smooth muscle antibody, a positive Raji-cell assay for immune complexes, and normal levels of IgG, IgM, and IgA. IgG subclasses revealed an IgG1 of 1225 (normal for age, 280-1120 mg/dl), IgG2 of less than 10 (30-630 mg/dl), IgG3 of 36 (40-250 mg/dl), and IgG4 of less than 4 (11-620 mg/dl). No increase in antibody titer was noted to either Pneumovax or unconjugated Haemophilus influenzae vaccine. Numbers of circulating B cells (CD19) were markedly diminished (less than 0.5%). Liver biopsies have shown chronic active hepatitis. Somatomedin C was 0.28 U/ml (normal for age, 0.5-2.06 U/ml). Challenge with either L-dopa or clonidine produced a peak GH response of 2.3 ng/ml (normals = greater than 7 ng/ml). Children with autoimmune disorders should be evaluated for IgG subclass deficiencies and ability to make antibody in response to antigen challenge regardless of the serum immunoglobulin levels. Growth failure in immune-deficient children should not be assumed to be due to chronic illness or recurrent infections. Other etiologies for growth failure should be sought.
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PMID:Association of autoimmunity with IgG2 and IgG4 subclass deficiency in a growth hormone-deficient child. 208 46


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