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 influence of cefodizime (CDZ) on CD4 and CD8 lymphocytes was investigated in patients with lower respiratory tract infection and underlying respiratory diseases. Ten men and one woman were treated with CDZ 1 g i.m. b.i.d. for ten days. The infecting organisms were Haemophilus influenzae (5), Streptococcus pneumoniae (2) and Escherichia coli (1). No adverse events were reported. Nine patients were clinically cured; two required further antibiotic therapy. Leucocyte counts decreased significantly during treatment. Lymphocyte counts and CD4 cells both increased significantly in absolute and relative numbers, while there was a much smaller increase in CD8 cells. This resulted in a significant increase in the CD4/CD8 ratio. These effects of CDZ might be of benefit for immunocompromised patients with bacterial infections.
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PMID:Changes in lymphocyte subpopulations in patients treated with cefodizime for acute lower respiratory tract infections. 152 80

3 splenectomized patients infected by the human immunodeficiency virus (HIV) are described. They all presented with more than 500 CD4/mm3 but, surprisingly, with a CD4 percentage below 15, positive p24 antigenemia and a CD4/CD8 ratio below 0.24. 2 patients had repeated episodes of oropharyngeal candidiasis while their CD4 counts exceeded 800/mm3. These episodes suggested the presence of a certain degree of immuno-suppression and prompted us to introduce anti-HIV therapy. 2 patients also presented with a pulmonary infection, due to Klebsiella pneumoniae and Haemophilus influenzae respectively. The third patient had septicemia due to Streptococcus pneumoniae type 22, despite vaccination and a CD4 count above 700/mm3. In splenectomized HIV-infected patients the number of CD4 lymphocytes should be interpreted with caution, as this number increases after splenectomy. The CD4 percentage and CD4/CD8 ratio correlated better with the clinical stage of HIV infection and gave more valuable indications as to the degree of immunosuppression. A possible correlation between viremia and the number of CD4 lymphocytes in this subset of patients remains to be established. In HIV-infected patients, infections due to S. pneumoniae, H. influenzae, S. aureus and enteric gram-negative bacteria are frequent. After splenectomy, susceptibility to encapsulated bacteria increases even in HIV-negative patients. Early vaccination against the main strains of S. pneumoniae is essential, as vaccinal response is uncertain in patients with less than 400 CD4/mm3.
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PMID:[HIV infection and splenectomy: 3 cases and literature review]. 892 55

We have previously shown that tonsil tissue both from children with tonsillar hypertrophy and recurrent tonsillitis is colonized and invaded by Haemophilus influenzae and Streptococcus pyogenes group A. In order to evaluate if these bacteria are involved in the immunopathogenesis of these two conditions, tonsillar cells from both groups were stimulated in vitro with intact, heat-inactivated H. influenzae or S. pyogenes A. The immunoreactivity was evaluated by assessing the induction of cytokine production (IL-1 alpha, IL-1 beta, TNF-alpha, IL-6, IL-8, IL-2, IFN-gamma, IL-4, TNF-beta and IL-10), which was detected at the single-cell level. All cytokines studied except IL-4 were induced in both groups after stimulation with H. influenzae or S. pyogenes A. The dominating cytokines were IL-1 beta, IFN-gamma and TNF-beta. No major differences in the cytokine pattern or number of cytokine-producing cells were noticed between the two patient cohorts after H. influenzae stimulation. Activation by S. pyogenes A bacteria gave rise to higher frequencies of IFN-gamma- and TNF-beta-synthesizing cells in the recurrent tonsillitis group. The incidence of CD4-, CD8-positive T cells and CD40-positive B cells was comparable between the two groups while the MAC-387-positive macrophages were significantly higher in the recurrent tonsillitis groups. In conclusion, a Th1 type of cytokine response was found in both groups following stimulation with H. influenzae or S. pyogenes A.
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PMID:Haemophilus influenzae and Streptococcus pyogenes group A challenge induce a Th1 type of cytokine response in cells obtained from tonsillar hypertrophy and recurrent tonsillitis. 951 80

Human CD1 is a family of nonpolymorphic major histocompatibility complex class I-like molecules capable of presenting mycobacterial lipids, including lipoarabinomannan (LAM), to double-negative (DN; CD4(-) CD8(-)) as well as CD8(+) T cells. Structural similarities between LAM and the capsular polysaccharides of gram-negative bacteria led us to consider the latter as candidate CD1 ligands. We derived two CD1-restricted DN T-cell populations which proliferated to Haemophilus influenzae type b (Hib) antigen. One T-cell population also proliferated to proteinase K-treated Hib antigen, suggesting that it recognized a nonpeptide. Our work thus expands the universe of T cell antigens to include nonpeptides distinct from mycobacterial lipids and suggests a potential role for CD1-restricted T cells in immunity to Hib.
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PMID:CD1 presents antigens from a gram-negative bacterium, Haemophilus influenzae type B. 967 29

Inflammation is essential to repair tissue damaged by physical, microbial or allergic mechanisms. Inappropriately zealous responses lead to destructive pathology or chronic disease cycles, whereas ideal outcomes are associated with complete and rapid restoration of tissue structure and function. The establishment of a rodent model investigating the different immune responses to non-typeable Haemophilus influenzae infection in both the lung and the ear indicate an ability to clear bacteria and reduce inflammation following mucosal immunisation. Lung histochemistry, upregulaion of macrophages and polymorphonuclear neutrophils, recruitment of gammadelta(+) and CD8(+) T cells, cytokine levels and depletion studies all support the hypothesis that mucosal immunisation facilitates control of the immune response resulting in enhanced bacterial clearance and programming of inflammation which limits damage and promotes the rapid restoration of structural normality.
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PMID:Programmed inflammatory processes induced by mucosal immunisation. 1125 87

Patients undergoing hematopoietic stem cell transplantation (HSCT) experience a prolonged period of dysfunctional immunity associated with an increased risk of bacterial and viral infections. Effective approaches toward vaccinating patients against common pathogens are being explored but are limited by poor levels of responsiveness. Relevant studies examining the nature of reconstitution of cellular and humoral immunity and its impact on vaccination strategies against infectious pathogens are reviewed. Following transplantation, deficiencies in cellular immunity are characterized by the inversion of CD4/CD8 ratios, a decreased proliferative response to mitogens, and the development of anergy to recall antigens as measured by delayed-type hypersensitivity testing. The impact on humoral immunity consists of decreased levels of circulating immunoglobulin, impaired immunoglobulin class switching, and a loss of complexity in immunoglobulin gene rearrangement patterns. In this setting, a loss of protective immunity has been demonstrated against viral and bacterial pathogens previously targeted by childhood vaccination. Infections due to encapsulated bacterial organisms such as Streptococcus pneumoniae and Haemophilus influenzae type B remain prevalent even in the late posttransplantation period. The efficacy of vaccination following HSCT is influenced by the time elapsed since transplantation, the nature of the hematopoietic graft, the use of serial immunization, and the presence of graft-versus-host disease. Strategies to enhance vaccine efficacy include pretransplantation immunization of the stem cell donor and the use of cytokine adjuvants.
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PMID:Vaccination against infectious disease following hematopoietic stem cell transplantation. 1130 51

The duration of immunodeficiency following marrow transplantation is not known. Questionnaires were used to study the infection rates in 72 patients surviving 20 to 30 years after marrow grafting. Furthermore, in 33 of the 72 patients and in 16 donors (siblings who originally donated the marrow) leukocyte subsets were assessed by flow cytometry. T-cell receptor excision circles (TRECs), markers of T cells generated de novo, were quantitated by real-time polymerase chain reaction. Immunoglobulin G(2) (IgG(2)) and antigen-specific IgG levels were determined by enzyme-linked immunosorbent assay. Infections diagnosed more than [corrected] 15 years after transplantation occurred rarely. The average rate was 0.07 infections per patient-year (one infection every 14 years), excluding respiratory tract infections, gastroenteritis, lip sores, and hepatitis C. The counts of circulating monocytes, natural killer cells, B cells, CD4 T cells, and CD8 T cells in the patients were not lower than in the donors. The counts of TREC(+) CD4 T cells in transplant recipients younger than age 18 years (at the time of transplantation) were not different from the counts in their donors. In contrast, the counts of TREC(+) CD4 T cells were lower in transplant recipients age 18 years or older, even in those with no history of clinical extensive chronic graft-versus-host disease, compared with their donors. The levels of total IgG(2) and specific IgG against Haemophilus influenzae and Streptococcus pneumoniae were similar in patients and donors. Overall, the immunity of patients surviving 20 to 30 years after transplantation is normal or near normal. Patients who received transplants in adulthood have a clinically insignificant deficiency of de novo-generated CD4 T cells, suggesting that in these patients the posttransplantation thymic insufficiency may not be fully reversible.
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PMID:Immunity of patients surviving 20 to 30 years after allogeneic or syngeneic bone marrow transplantation. 1173 50

We describe herein a case of nephrotic syndrome (NS) following allogeneic bone marrow transplantation (allo-BMT) for natural killer cell leukemia/lymphoma. Histologic studies defined the diagnosis as crescentic glomerulonephritis with massive immunoglobulin A (IgA) deposition, which has never been reported in NS cases following allo-BMT. Most of the massive infiltrated cells in the interstice were CD3(+)CD4(-)CD8(+) T cells derived from the donor. We observed mesangial deposition of Haemophilus parainfluenza outer membrane (OMHP) antigen and decreased glycosylation of the IgA1 hinge in the recipient's samples is consistent with the recently reported pathogenesis of IgA nephropathy. Further, the titer of IgA antibody against the donor serum was as high as other IgA nephropathy cases. These findings suggest that NS and crescentic glomerulonephritis in this case occurred as one of the forms of chronic graft-versus-host disease (GVHD), and that IgA deposition was associated with H parainfluenza and decreased glycosylation of the IgA1 hinge.
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PMID:Nephrotic syndrome with crescent formation and massive IgA deposition following allogeneic bone marrow transplantation for natural killer cell leukemia/lymphoma. 1254 67

A 32-year-old male was admitted to our hospital complaining of fever and dyspnea on effort. Laboratory data on admission indicated leukocytosis and elevation of C-reactive protein. A chest radiograph showed diffuse reticulonodular shadows in both lower lung fields, and a chest computed tomography showed centrilobular reticulonodular opacity. Bronchoscopic findings revealed a large amount of slightly yellowish secretion in all bronchi. Cells found in the bronchoalveolar lavage fluid (BALF) included 61% neutrophils. Haemophilus influenzae was isolated from cultures of the BALF and sputum. Transtracheal lung biopsy specimens showed focal infiltration of neutrophils in the alveoli, and the pathological findings in the lung were compatible with bronchiolopneumonia. Since the CD4/CD8 ratio was 0.09 and a positive reaction was obtained for anti-human immunodeficiency virus (HIV) antibody, HIV-associated pneumonia due to H. influenzae was diagnosed. Seven days' administration of cefozopran improved the patient's condition. It is interesting that radiological findings are often unusual in HIV-infected patients with H. influenzae pneumonia.
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PMID:[A case of AIDS-associated Haemophilus influenzae pneumonia with diffuse reticulonodular shadows]. 1264 13

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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