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 frequency of precipitating antibody to heat-labile (H(1--2) and heat-stable (HCW and HCF) antigens of Haemophilus influenzae was determined in patients with asthma, chronic bronchitis, cystic fibrosis and bronchiectasis and compared with that in a control group. This showed that the immune response of asthmatic patients to heat-stable antigens was different from that to the heat-labile antigens. Exposure to antigens of H. influenzae is common in all the disease groups. Skin test reactions having the time course and macroscopic appearance of Type I (immediate) and Type III (late) were obtained after prick and intracutaneous skin testing with HCW antigen in varying concentrations in a group of patients with asthma, chronic bronchitis or cystic fibrosis and in a control group. It is suggested that IgE and short-term sensitizing IgG antibodies may be responsible for the immediate reactions while activation of the alternative pathway of complement by endotoxin contained in HCW could be responsible for the late reactions. HCW antigens were shown to release histamine from non-sensitized human leucocytes; HCW and HCF antigens were shown to release histamine from non-sensitized human lung. None of the antigens tested had an effect on beta-receptors in tracheal preparations. It is proposed that these reactions may contribute to the pathogenicity of H. influenzae in the lower respiratory tract.
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PMID:In vivo and in vitro reactions to antigens of Haemophilus influenzae in bronchial obstruction. 9 81

Studies of IgG, IgA, IgM and IgE in serum and of IgG, IgA and IgM in saliva were performed in 52 children undergoing tonsillectomy. The results revealed that levels of IgA in serum and saliva in the patients were significantly reduced as compared with levels in age- and sex-related healthy controls (p less than 0.001 and less than 0.025 respectively). Recovery of beta-haemolytic streptococci and Haemophilus influenzae from the removed tonsils was also well correlated with low IgA in serum (p less than 0.01). A considerable lack of IgA fluorescing plasma cells in tonsillar tissue demonstrated in an earlier study of the same patients was consistent with carriage of beta-haemolytic streptococci and Haemophilus influenzae (p less than 0.01). The significant decrease in serum- and saliva IgA was only found among the youngest patients in this study. The hypothesis is raised that the decreased level of saliva IgA influences the increased tendency at pathogenic bacteria to adhere to and colonize on the tonsil mucosa, and furthermore, the lack of IgA plasma cells in the tonsils supports the view that IgA prevents penetration of microorganisms through the epithelial surface, secondarily establishing an acute inflammation of the tonsils.
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PMID:IgA levels and carrier rate of Haemophilus influenzae and beta-haemolytic streptococci in children undergoing tonsillectomy. 78 44

Haemophilus influenza and its extracellular products (EP) did not release histamine from basophil leukocytes in cell suspensions from normal individuals, patients with chronic bronchitis or patients allergic to either house dust mite, grass pollen, cat dander or to their own bacteria. However, the EP was found to enhance their basophil histamine release. IgE-mediated histamine release was examined by stimulation of the cells with anti-IgE or the specific allergens, and non-immunological histamine release by stimulating the cells with the calcium ionophore A23187 or Staphylococcus aureus. In all the experiments EP caused a significant increase in the histamine release. When H. influenzae endotoxins were removed from the EP, the potentiating effect of EP was completely abolished, whereas heating (80 degrees C, 30 min) or treatment of EP with proteinase did not influence the potentiating effect. These results indicate that H. influenzae endotoxin potentiates histamine release caused by IgE-mediated reactions or by non-immunological mechanisms.
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PMID:Endotoxin from Haemophilus influenzae enhances IgE-mediated and non-immunological histamine release. 168 72

Haemophilus influenzae and its extracellular products (EP) did not release histamine in leukocyte suspensions from normal individuals. However, the EP were found to enhance basophil histamine release triggered by anti-IgE and by the calcium ionophore A23187. Experiments with EP indicate that it is the content of endotoxins which is responsible for the potentiating effect. Removal of endotoxin from the EP thus completely abolished the potentiating effect, whereas inactivation of its protease and proteins by heat-treatment or by proteinase K did not change the potentiation. A reinforcement of mediator release by the extracellular products of H. influenzae might play a pathophysiological role in chronic obstructive pulmonary disease.
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PMID:Haemophilus influenzae potentiates basophil histamine release possibly by its endotoxins. 169 61

To investigate whether an underlying defect in antibody (Ab)-forming capacity could contribute to the infection susceptibility of patients with hyper-IgE syndrome, we evaluated 11 such patients for their responses to bacteriophage phi X174 (phi X174), diphtheria and tetanus toxoids, and pneumococcal (Pneumovax) and Hemophilus influenzae vaccines. Three of nine patients immunized with phi X174 had normal primary and secondary Ab responses, five had accelerated declines in their titers after initially normal primary Ab responses and lower than normal secondary Ab responses, and two of the latter patients failed to switch normally from IgM to IgG Ab production. Only one of 10 patients tested had normal Ab responses to diphtheria toxoid, and postimmunization antitetanus titers were abnormally low in five of the 10 patients tested. Serum Abs to H. influenzae polyribose phosphate were protective in seven of the eight immunized patients. Five of the nine patients administered Pneumovax had poor Ab responses to at least one of the pneumococcal serotypes 7, 9, or 14. Abnormal antipolysaccharide responses did not correlate with IgG2 deficiency. All patients responded with protective Ab levels to type 3. Thus, patients with hyper-IgE syndrome are heterogeneous with respect to their Ab-forming capacities. Ab deficiency may contribute to infection susceptibility in some of these patients.
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PMID:Antibody responses to protein, polysaccharide, and phi X174 antigens in the hyperimmunoglobulinemia E (hyper-IgE) syndrome. 182 6

Sixty-one patients with chronic sinusitis who were referred for an allergy evaluation were evaluated for immunologic competence including assessment of quantitative serum immunoglobulin levels, IgG subclass levels, and response to pneumococcal and Haemophilus influenzae vaccines. In addition to chronic sinus disease, recurrent otitis media and asthma exacerbation were common problems in this group. Five patients had an elevated age-adjusted IgE level and 22 patients had positive prick tests to one or more environmental inhalants; these findings suggest an allergic component in this subgroup. Twelve additional patients had highly reactive intradermal tests to common environmental allergens, which also may be clinically significant for underlying atopy. Eleven patients had low immunoglobulin levels, 6 had low immunoglobulin levels and vaccine hyporesponsiveness, and 17 had poor vaccine response only. Thus, 34 of 61 patients with refractory sinusitis had abnormal results on immune studies, with depressed IgG3 levels and poor response to pneumococcal antigen 7 being most common. In addition to allergy, immunologic incompetence may be an important etiologic factor in patients with chronic, refractory sinusitis.
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PMID:Immunologic defects in patients with refractory sinusitis. 194 19

Protein D, a novel surface protein of the bacterial species Haemophilus influenzae with affinity for human IgD, was isolated after solubilization with sonication and Sarcosyl-extraction by a single SDS-PAGE step. From 1 ml of packed bacteria was prepared 0.25 mg of purified protein D. The apparent m.w. of protein D was estimated to 42,000 by SDS-PAGE and gel chromatography. Edman degradation cycles of protein D produced no amino acid phenylthiohydantoin derivatives and the amino-terminal end of the single protein D polypeptide chain is thus probably blocked. Protein D differs from all previously described outer membrane proteins (protein 1 to 6) of H. influenzae. Thus, protein D did not react with antibodies against protein 1 or protein 2 and the latter proteins did not bind IgD. Protein D was found to exhibit unique Ig-binding properties. Thus, in dot blots protein D bound four different human IgD myeloma proteins but not IgG, IgM, IgA, IgE, or some additional proteins. On the IgD molecule, constant parts of the H chains both in the Fab and Fc fragments appear responsible for the interaction with protein D. This novel Ig-binding reagent promises to be of theoretical and practical interest in immunologic and microbiologic research.
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PMID:Protein D of Haemophilus influenzae. A novel bacterial surface protein with affinity for human IgD. 223 Jan 24

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

We report a case of Burkitt's lymphoma developing in a 7-year-old boy with hyper-IgE syndrome. This is the third reported case of malignancy in the hyper-IgE syndrome. The other two cases were an 18-year-old man with Hodgkin's disease and a 10-year-old girl with histiocytic lymphoma. The patient developed retroperitoneal Burkitt's lymphoma with probable metastasis to the brain. His short life was characterized by recurrent staphylococcal skin, middle ear, and lung infections associated with extremely elevated serum concentrations of IgE. There was also an associated disturbance of bone metabolism with osteoporosis and pathologic fractures and absence of parathormone, findings that have been observed in other patients with hyper-IgE syndrome and other forms of T cell immunodeficiency. At the age of 5 years, inadequate B cell responses to immunization with antigens derived from diphtheria, tetanus, and Haemophilus influenzae type b organisms and with the OX174 bacteriophage were demonstrated in the patient. In his terminal state his in vitro lymphocyte analysis demonstrated findings of anergy. Although the precise immunologic defect in hyper-IgE syndrome is unknown, these cases of associated malignancy stress the role that a completely normal immune system plays in preventing the premature appearance of cancer.
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PMID:Burkitt's lymphoma developing in a 7-year-old boy with hyper-IgE syndrome. 278 97

We report a 5-year-old girl with adenosine deaminase (ADA) deficiency who was asymptomatic during the first years of life. At 3 years of age, she developed chronic and recurrent sinopulmonary infections, and at 4 1/2 years of age she had one major infection with Streptococcus pneumoniae (bacteremia and septic arthritis of the hip). Immunologic evaluation at 5 years of age revealed persistent lymphopenia, decreased helper-suppressor T cell ratios, and low proliferative responses to mitogens. The IgG, IgM, and IgA levels were normal; the IgG2 level was low normal or below normal. The patient had specific antibodies against toxoids and viral antigens but failed to produce antibodies against Haemophilus influenzae type b and pneumococcal polysaccharides. Although no symptoms of allergy were present, she had persistent eosinophilia and elevated IgE levels. The patient had 0.6% of normal ADA activity in erythrocytes and approximately 1% of normal ADA activity in peripheral blood mononuclear cells. Beginning at 6 years of age, she was treated with weekly injections of polyethylene glycol-modified bovine ADA. This treatment was well tolerated and effectively reversed the biochemical consequence of ADA deficiency. Concomitantly, she improved clinically and her T lymphocyte numbers and blastogenic responses to mitogens in vitro became normal. The late onset of clinical symptoms and relatively benign clinical course in this patient emphasize the need to consider ADA deficiency in a broad spectrum of immunodeficient children.
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PMID:Adenosine deaminase deficiency with late onset of recurrent infections: response to treatment with polyethylene glycol-modified adenosine deaminase. 326 Sep 44


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