LPS inhibits the intracellular growth of Legionella pneumophila in thioglycolate elicited murine peritoneal macrophages by iron-dependent, tryptophan-independent, oxygen-independent, and arginine-independent mechanisms
| Autor: | Thomas W. Klein, Yoshimasa Yamamoto, S J Gebran, Herman Friedman, Mitsugu Tomioka, Ray Widen, Catherine Newton |
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| Rok vydání: | 1995 |
| Předmět: |
Lipopolysaccharides
Lipopolysaccharide Mice Inbred A Nitrogen Iron Immunology Transferrin receptor Arginine Legionella pneumophila Microbiology Superoxide dismutase Mice chemistry.chemical_compound Receptors Transferrin Animals Immunology and Allergy Macrophage Drug Interactions Cells Cultured chemistry.chemical_classification biology Tryptophan Cell Biology biology.organism_classification Oxygen chemistry Transferrin Thioglycolates Macrophages Peritoneal biology.protein Female Growth inhibition Reactive Oxygen Species Intracellular |
| Zdroj: | Journal of Leukocyte Biology. 57:80-87 |
| ISSN: | 1938-3673 0741-5400 |
| DOI: | 10.1002/jlb.57.1.80 |
| Popis: | Thioglycolate-elicited murine macrophages from genetically susceptible A/J mice activated with lipopolysaccharide (LPS) and infected with Legionella pneumophila in vitro evince marked inhibition of intracellular growth of this bacterium. The mechanism of inhibition by LPS-activated macrophages in terms of replication of this intracellular pathogen is unclear. LPS activation of murine macrophages induced a downshift in transferrin receptor (TfR) expression and reduction in cellular iron content, and this was correlated with augmented intracellular growth of Legionella in the cells. When LPS-stimulated macrophages were first saturated with iron, partial reversion of L. pneumophila growth restriction was observed. However, an excess of exogenous L-tryptophan (Trp) did not reverse this growth inhibition, nor did supplementation of the macrophage culture medium with both iron and Trp. The antilegionella activity of the macrophages induced by LPS activation was independent of reactive oxygen intermediates (ROI), since the scavengers catalase, superoxide dismutase, mannitol, and thiourea had no effect on growth restriction. Likewise, notwithstanding the ability of LPS-activated macrophages to synthesize reactive nitrogen intermediates (RNI), which was inhibited by l-arginine analogs (NG-monomethyl-l-arginine and l-aminoguanidine), as well as by incubation in arginine-free medium, their ability to inhibit the intracellular replication of L. pneumophila was not affected. Thus, we conclude that LPS-activated macrophages inhibit the intracellular growth of L. pneumophila partially by iron-dependent, Trp-independent, and ROI- and RNI-independent mechanisms. We also suggest that additional unknown mechanisms are involved, since complete reversion was not obtained. J. Leukoc. Biol. 57: 80–87; 1995. |
| Databáze: | OpenAIRE |
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