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)

Patients with the hyper-IgE (HIE) syndrome have recurrent bacterial infections with Staphylococcus aureus and other polysaccharide encapsulated organisms. To determine whether an impairment of the antibody response to polysaccharide antigens contributes to infections in this syndrome, we measured serum antibody to the teichoic acid of S. aureus and to the capsular polysaccharide of Haemophilus influenzae type b. Compared to control subjects who had no history of S. aureus infections (N = 14), sera from patients with HIE (N = 9) lacked the expected elevation of serum antibody to teichoic acid (p greater than 0.05) and had significantly lower levels of this antibody than sera from 14 patients with atopic dermatitis, complicated by recurrent cutaneous S. aureus infections (p less than 0.01). After immunization with the capsular polysaccharide of Haemophilus influenzae type of vaccine, the antibody response of patients with HIE was significantly impaired compared to that of age-matched control subjects (p = 0.01). Although patients with HIE syndrome had normal total IgG levels, most patients with HIE but not patients with atopic dermatitis had IgG2 subclass deficiency. Defective antibody responses in patients with HIE were not restricted to polysaccharide antigens because the serum levels of antitetanus toxoid antibody in these patients were significantly lower than that of control subjects (p less than 0.001). Impaired antigen-specific antibody responses in patients with HIE syndrome may contribute to their increased susceptibility to infection.
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PMID:Impaired antibody responses in the hyperimmunoglobulin E syndrome. 337 21

Among 586 children with asthma, 484 (82%) were found to have IgE-mediated ("extrinsic") asthma, and seventy-two (12%) non-IgE ("intrinsic") asthma. The remaining 30 patients (6%) were classified as "intermediate", as they had serum IgE within or above serum IgE levels of healthy children but no allergy to common allergens. During a three-year study period, the seventy-two patients with intrinsic asthma as opposed to 84 patients with extrinsic asthma had significantly more hyperinflation of the lungs, more episodes of acute hospital admissions due to asthma and/or pneumonia, more elevated serum IgG and IgM, and more cultures from secretions of lower airways of Haemophilus influenzae and pneumococci. Further, although treated with corticosteroids, eleven of the children with intrinsic asthma showed progressive disease, judged from fixed and/or declining forced vital capacity followed by signs of lung fibrosis on repeated pulmonary X-rays. It is emphasized that children with intrinsic asthma may represent an entity of childhood asthma, in some cases with severe progression of disease within a few years.
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PMID:Non-IgE-mediated asthma in children. 405 Apr 18

The hyperimmunoglobulin E recurrent-infection syndrome (HIE) entails a disorder of recurrent bacterial infections of the skin and sinopulmonary tract commencing in infancy or early childhood in the presence of serum levels of IgE which are at least 10 times normal (greater than 2,000 IU/ml). Variable concomitants of HIE are coarse facies, chronic eczematoid rashes, cold cutaneous abscesses, mild eosinophilia, mucocutaneous candidiasis, and a neutrophil chemotactic defect. The bacteria which commonly infect these patients are Staphylococcus aureus and Haemophilus influenzae although Streptococcus pneumoniae and enteric gram-negative rods are seen in some cases. Other than pneumonias, deep-seated infections are unusual, although osteomyelitis, arthritis, and visceral abscesses are seen. Bacteremia and sepsis are rare. Therapy should involve prolonged intravenous antibiotics and early surgery to treat infections which usually seem deceptively benign. HIE patients' neutrophils display a variable chemotactic defect, and their mononuclear cells variably produce an inhibitor of neutrophil chemotaxis. The production of the inhibitor correlates with the in vitro chemotactic defect. The basis of the propensity for recurrent infections is still speculative, and the further study of this syndrome should add new dimensions to our understanding of host defenses against bacterial invaders.
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PMID:The hyperimmunoglobulin E recurrent-infection (Job's) syndrome. A review of the NIH experience and the literature. 634 70

Bacterial respiratory infections, especially with Haemophilus influenzae and Streptococcus pneumoniae, are frequently associated with an increase of airways obstruction in patients with bronchial asthma. The possible involvement of immediate hypersensitivity in this phenomenon was studied. IgE antibodies to Haemophilus influenzae (HI) and Streptococcus pneumoniae (SPn) were investigated in the serum of 190 adult patients with bronchial asthma. The IgE antibodies were measured using a solid phase radioimmunoassay method. Living bacteria were used as solid phase. A correction of the non-specific binding of IgE was necessary. IgE antibodies to one or both bacteria were present in 55 of the 190 patients (29%). Eighteen patients were sensitive to HI, 33 to SPn and four to both bacteria. Significantly more IgE antibodies to bacteria were found in patients with demonstrable IgE antibodies to various inhalant allergens. However, the IgE antibodies to one or both bacteria were also present in 22% of patients with no other demonstrable IgE mediated hypersensitivity. The total serum IgE level in patients with IgE antibodies to bacteria was not significantly higher than in patients without hypersensitivity to these bacteria. From these data we concluded that immediate hypersensitivity to bacteria may play a role in the infectious exacerbations of bronchial asthma.
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PMID:IgE antibodies to bacteria in patients with bronchial asthma. 697 85

A radio-allergosorbent test (RAST) to measure specific IgE antibodies in man to whole bacterial cells of Streptococcus pneumoniae, Staphylococcus aureus and Haemophilus influenzae was developed to investigate different well-defined lung diseases (chronic bronchitis, allergic bronchopulmonary aspergillosis (ABPA), bronchial asthma allergic rhinitis, cystic fibrosis) and also in urticaria as compared with non-atopic blood donors. In addition, total IgE values and skin prick tests were assessed in these patients. The ABPA group gave the highest specific IgE RAST scores to all three bacteria, whilst the chronic bronchitis and cystic fibrosis groups also gave raised RAST scores with H. influenzae. There was a positive correlation between the patients' Sta. aureus and Str. pneumoniae immediate-type skin reactions and their RAST scores and total serum IgE concentrations, but there was only a low incidence of immediate-type skin test positivity to H. influenzae.
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PMID:Specific serum IgE antibodies to bacterial antigens in allergic lung disease. 698 89

The respiratory mucosa is protected primarily by a secretory immune system that is under complex and only partly understood immunoregulatory control. Secretory immunoglobulins (SIgA and SIgM) protect the mucosal surface by immune exclusion of antigens. However, the fact that most IgA produced in the respiratory tract belongs to the IgA1 subclass renders SIgA in this region susceptible to IgA-specific proteases produced by Haemophilus influenzae, Streptococcus pneumonia, and Neisseria meningitidis. Immunoglobulin G can also perform immune exclusion at respiratory surfaces but, like IgE, it reaches the secretions merely by passive diffusion. The phlogistic properties of antibodies belonging to these classes explain their potential involvement in maintaining mucosal inflammation. In patients with selective IgA deficiency, SIgA is lacking and is not regularly compensated for satisfactorily by SIgM. In such patients unexplained immunoregulatory mechanisms, perhaps involving the local microbiota, give rise to a large number of IgD-producing cells in the upper respiratory tract. Immunoglobulin D cannot act as a secretory antibody and might block the protective properties of IgG; this could explain why these patients are particularly prone to recurrent infections. Our observations show that there are large individual variations in the mucosal immune system with regard to humoral immunity in the upper respiratory tract.
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PMID:The role of humoral mucosal immunity in the induction and maintenance of chronic airway infections. 776 61

Haemophilus influenzae (H. influenzae), Streptococcus pneumoniae (S. pneumoniae) and Branhamella catarrhalis (B. catarrhalis) are often found in the lower respiratory tract of patients with chronic bronchitis. Earlier studies have shown that bacteria induce mediator release from human basophils and parenchymal lung mast cells. In this study the capability of bacteria to trigger or potentiate histamine release from superficially located mast cells in the airway epithelium was studied in cell suspensions obtained by bronchoalveolar lavage in patients with chronic bronchitis (CB). In approximately half of the patients H. influenzae and Staphylococcus aureus (S. aureus) were found to trigger histamine release, whereas no response was obtained by S. pneumoniae or B. catarrhalis. The mediator release was caused by a non-IgE-dependent mechanism. At lower concentrations of H. influenzae causing no histamine release the bacterium was found to enhance IgE-mediated histamine release triggered by anti-IgE antibody. The synergy was more pronounced in patients with CB than in controls. Since H. influenzae is found in the lower respiratory tract of the patients but not in normal individuals, the infection here may via histamine release lead to harmful effects on the airways of importance for precipitation and exacerbation of chronic bronchitis.
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PMID:Haemophilus influenzae release histamine and enhance histamine release from human bronchoalveolar cells. Examination of patients with chronic bronchitis and controls. 854 45

The investigation includes 12 patients hospitalized with acute exacerbations of chronic bronchitis (CB) and infected in the lower respiratory tract with Haemophilus influenzae (HI) or Streptococcus pneumoniae (SP). Eight patients were infected the HI, three with SP, and one patient with both species. Basophil-bound IgE and serum IgE directed against these species were examined using the patients' own bacterial isolates. All patients showed IgE-mediated histamine release when their peripheral leukocytes were incubated in vitro with the infecting species, indicating basophil-bound IgE directed against their own bacterium. No IgE-mediated response was obtained in the control group of 12 healthy individuals. Bacteria-specific IgE in serum was demonstrated by immunofluorescence assay and further verified by passive sensitization. There was a positive serum titre in seven of nine patients housing HI and in all SP-infected patients but not in the control group. No synchronism was found between a positive response in the histamine release test and the immunofluorescence assay by parallel testing during the test period. This may be due to a time delay between production of serum IgE and its fixation to the cell surface. The results indicate a potential for a bacteria-specific IgE-mediated immune response in CB. Thus, by triggering mediator release, bacteria may be involved in the pathogenesis of exacerbations in CB.
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PMID:Basophil-bound IgE and serum IgE directed against Haemophilus influenzae and Streptococcus pneumoniae in patients with chronic bronchitis during acute exacerbations. 864 60

The fungal revolution taking place in otorhinology inspired us to study the frequency of occurrence of fungi in the nasal mucus of chronic rhinosinusitis (CRS) patients (with or without polyposis) in order to evaluate the incidence of eosinophilic fungal sinusitis in CRS patients. Ninety-six samples were examined from patients with CRS. In 74 cases mucus was collected non-invasively, and in 22 cases during operation. The Gram-stained direct smears of all samples were also evaluated. Bacteria and fungi colonizing in the mucus were detected by culturing method. The control group consisted of 50 healthy volunteers. Typical aerobic pathogenic bacteria could be isolated from 34 patients. Fifty-seven aerobic bacteria were isolated, i.e. 1.6 bacteria/positive patient with a maximum of 3 different bacteria/sample. The most frequently isolated bacteria were Staphylococcus aureus, Escherichia coli, Klebsiella pneumoniae, Streptococcus pneumoniae, and Haemophilus influenzae. Yeasts and moulds could be detected from 79 patients (83%): Candida albicans, Candida spp., Aspergillus spp., Cladosporium spp, and Penicillium spp. were isolated most frequently. Altogether 237 yeasts and moulds were isolated, i.e. 3.0 different fungi/positive patient, with a maximum of 5 different fungi/sample. In the control group aerobic pathogens were not isolated, only apathogenic species. Fungi were isolated from 22 healthy patients (44%). These data indicate that fungi are frequently involved in the aetiology of CRS. IgE-medicated hypersensitivity to fungal allergens could not be proven in our patients.
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PMID:Identification and incidence of fungal strains in chronic rhinosinusitis patients. 1210 67

Eleven Norwegian patients (aged 2-33 years, seven males and four females) with Ataxia-telangiectasia (A-T) and their parents were investigated. Five of the patients were homozygous for the same ATM mutation, 3245delATCinsTGAT, a Norwegian founder mutation. They had the lowest IgG2 levels; mean (95% confidence interval) 0.23 (0.05-0.41) g/l versus 0.91 (0.58-1.26) g/l in the other patients (P = 0.002). Among the 11 A-T patients, six had IgG2 deficiency, six had IgA deficiency (three in combination with IgG2 deficiency) and seven had low/undetectable IgE values. All patients had very low levels of antibodies to Streptococcus pneumoniae 0.9 (0.4-1.4) U/ml, while normal levels were found in their parents 11.1 (8.7-13.4) U/ml (P < 0.001). A positive linear relationship between pneumococcal antibodies and IgG2 (r = 0.85, P = 0.001) was found in the patients. Six of 11 had diphtheria antibodies and 7 of 11 tetanus antibodies after childhood vaccinations, while 4 of 7 Hemophilus influenzae type b (Hib) vaccinated patients had protective antibodies. Ten patients had low B cell (CD19+) counts, while six had low T cell (CD3+) counts. Of the T cell subpopulations, 11 had low CD4+ cell counts, six had reduced CD8+ cell counts, and four had an increased portion of double negative (CD3+/CD4-/CD8-) gamma delta T cells. Of the 22 parents (aged 23-64 years) 12 were heterozygous for the ATM founder mutation. Abnormalities in immunoglobulin levels and/or lymphocyte subpopulations were also observed in these carriers, with no correlation to a special ATM genotype.
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PMID:The impact of an early truncating founder ATM mutation on immunoglobulins, specific antibodies and lymphocyte populations in ataxia-telangiectasia patients and their parents. 1519 60


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