Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023241 (Legionella)
 6,990 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Preliminary estimation of virulence in some antibiotic resistant mutants of Legionella pneumophila, Philadelphia 1 in various models of infection revealed its decrease in the mutants resistant to azlocillin, cefotaxime, fluoroquinolone LIB-80, neamine and streptomycin. Detailed investigation of the neamine resistant mutants showed that in relation to streptomycin susceptibility such mutants could be divided into 3 classes: susceptible to streptomycin, resistant to high concentrations of streptomycin and resistant to moderate concentrations of streptomycin. Part of mutants Nea(r)Strr and Nea(r)Strr500 and all mutants Nea(r)Strr100 proved to be less virulent with respect to guinea pigs and chick embryos. The study of the spectinomycin resistant mutants of Legionella spp. did not reveal any changes in the virulence which made it possible to suggest that the influence of the mutations in the ribosomal protein genes determining resistance to streptomycin and neamine on virulence of L. pneumophila was based on the interdependence of the mutant effect on the suppression and the influence on the virulence detected by us in S. flexneri, Y. pseudotuberculosis, L. monocytogenes and F. tularensis. The Legionella mutants Nea(r)Strr100 were characterized by significant protective activity and protected immunized guinea pigs when tested in a model of their aerogenic infection.
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PMID:[Isolation and biological characterization of Legionella pneumophila mutants resistant to aminoglycoside antibotics and their protective action]. 941 1

The death of immune cells in response to pathogens often dictates the outcome of an infection. In some contexts, pathogens specifically kill immune cells by producing highly potent toxins or by triggering host cell death pathways, thus ensuring successful infections. But for intracellular pathogens and viruses, the death of host cells normally is disastrous for their intracellular life cycle. Our recent experiments with the pathogen Legionella pneumophila revealed that the bacterial ribosomal protein RpsL is able to trigger lysosomal membrane permeabilization (LMP) and the subsequent macrophage cell death. Interestingly, a lysine to arginine mutation at the 88th residue, which also confers resistance to the antibiotic streptomycin, substantially impaired the cell death inducing activity of RpsL and allowed L. pneumophila to succeed in intracellular replication, suggesting the convergence of resistance mechanisms to innate immunity and antibiotics. The discovery of lysosomal cell death as an immune response to a bacterial ligand has expanded the spectrum of reactions that host cells can mount against bacterial infection; these observations provide a model to study the pathways that lead to the induction of LMP, a currently poorly understood cellular process involved in the development of many diseases.
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PMID:A new way to detect the danger: Lysosomal cell death induced by a bacterial ribosomal protein. 2605 50