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)

Macrolide antibiotics (Mac) consist of a 12- to 16-membered lactone ring combined with a sugar moiety, and they inhibit protein synthesis via binding to 23S ribosomal RNA in bacteria. The 14- and 16-membered Mac are used for treating infectious diseases caused by Gram-positive and other bacteria; e.g., Haemophilus influenzae, Bordetella pertussis, Legionella pneumophila, Campylobacter, Treponema pallidum and Mycoplasma. Resistance to macrolide, lincosamide, and streptogramin-B (MLS) antibiotics in staphylococci is known to have the following mechanisms: 1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the erm gene, and consequently a decrease in binding of MLS antibiotics; 2) inactivation of streptogramin-B (STG-B) and lincosamide by the products of the sbh (encoding streptogramin B hydrolase) and linA' (encoding 3-lincomycin 4-clindamycin O-nucleotidyltransferase) genes, respectively; and 3) active efflux of Mac and STG-B antibiotics determined by the msrA and msrB genes in Staphylococcus epidermidis and Staphylococcus xylosus, respectively, both of which appear to act as an ATP-dependent efflux pump. I have shown that Staphylococcus aureus 8325(pEP2104) exhibits inducible resistance to PMS (partial macrolide and streptogramin B)-antibiotics [the 14-membered macrolides, erythromycin (EM), and oleandomycin (OL), and the 16-membered macrolide mycinamicin (MCM) and STG-B]. The sequence of the N-terminal amino acid residues of a 63 kDa protein (MsrSA) that appeared in the membrane of PMS-resistant strains was identical to that of an MsrA polypeptide related to enhanced efflux of [14C]EM. Ribosomes from PMS-resistant strains showed a similar affinity for EM to those from the PMS-sensitive host strain NCTC8325, and no inactivation of EM by 8325(pEP2104) was observed. In the present study, I showed the DNA sequence of the msrSA region on the constitutive PMS-resistant plasmid pMC38, PMS-inducible resistant plasmid pEP2104 and PMS-sensitive mutant plasmid pSP6, and the region that is essential for inducible expression in PMS resistance. In addition, I investigated the relationship between PMS resistance and intracellular accumulation of EM.
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PMID:[Study of macrolide, lincosamide, and streptogramin B antibiotics resistance in Staphylococcus aureus]. 1077 59

The objective of this study was to evaluate humoral immunity of allergic respiratory children with chronic/recurrent sinusitis. Twenty-seven allergic respiratory (persistent mild/moderate asthma and persistent allergic rhinitis) children (7-15-year old) with chronic or recurrent sinusitis were evaluated. Patients had symptoms and abnormal computer tomography scan even after two adequate treatments (long-lasting antibiotics, decongestants, and short-term oral corticosteroids). clinical examination, sweat test, total blood cell count, measurement of serum levels of: total and specific IgE, immunoglobulins (G, M, A), IgG subclasses, antibodies to Haemophilus influenza type b (IgG anti-Ps Hib) and pneumococcal serotypes (IgG anti-Ps 1, 3, 5, 6B, 9V, and 14) before and after active immunization (Act-Hib and Pneumo23, Aventis Pasteur SA, Lyon, France), Rubella neutralizing antibody titers and human immunodeficiency virus antibodies. Specific IgE to inhalant allergens higher than class III were observed in 24/27 patients. One patient had IgA plus IgG2 deficiency and other an IgG3 deficiency. Eight and 12 of 27 patients had IgG2 and IgG3 serum levels below 2.5th percentile, respectively. Immunological responses to protein and polysaccharide antigens were normal in all patients. Although our patients have been appropriately treated of their allergic diseases, they persisted with chronic/recurrent sinusitis and 60% of them had a documented osteomeatal complex blockade. In spite of the diagnosis of IgA plus IgG2 deficiency and an isolated IgG3 deficiency, in all patients an adequate response to Ps antigens was observed. Primary and/or secondary humoral immunodeficiency seems not to be the main cause of chronic/recurrent sinusitis in patients with respiratory allergic disease.
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PMID:Immunological evaluation of allergic respiratory children with recurrent sinusitis. 1617 2