Lack of microbicidal response in human macrophages infected with Parachlamydia acanthamoebae

Détails

ID Serval
serval:BIB_A9812D3E27D6
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Lack of microbicidal response in human macrophages infected with Parachlamydia acanthamoebae
Périodique
Microbes and Infection
Auteur⸱e⸱s
Greub  G., Desnues  B., Raoult  D., Mege  J. L.
ISSN
1286-4579 (Print)
Statut éditorial
Publié
Date de publication
04/2005
Volume
7
Numéro
4
Pages
714-9
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Apr
Résumé
Parachlamydia acanthamoebae is an obligate intracellular bacterium naturally infecting free-living amoebae. This potential agent of pneumonia resists destruction by human macrophages, inducing their death by apoptosis. However, the strategy used by Parachlamydia to escape the microbicidal effectors of macrophages remains unknown. In this work, we defined the effect of Parachlamydia on the cytokine secretion (measured in culture supernatants by immunoassays), on the oxidative burst (measured using a fluorogenic probe), on the production of nitric oxide (Griess assay), and on transcription of glutaredoxin, tumor necrosis factor alpha (TNF-alpha) and indoleamine 2,3-dioxygenase (IDO). Living Parachlamydia did not induce an oxidative burst, the secretion of cytokines such as IL-6, IL-10 and TNF-alpha, nor the transcription of TNF-alpha in macrophages. However, living Parachlamydia led to increased secretion of IL-1beta and increased transcription of glutaredoxin, an anti-oxidant. The transcription of IDO, an enzyme, which catalyzes decyclization of l-tryptophan, was slightly up-regulated. Heat-inactivated Parachlamydia did not induce either an oxidative burst or the production of pro-inflammatory cytokines. In contrast to living bacteria, it had no effect on the IL-1beta release, but it induced IL-10 secretion. In conclusion, after being internalized, Parachlamydia may resist the microbicidal effectors of human macrophages through not inducing oxidative burst and pro-inflammatory cytokine production.
Mots-clé
Acanthamoeba/*microbiology Animals Chlamydiales/immunology/*pathogenicity Cytokines/metabolism Down-Regulation Humans Indoleamine-Pyrrole 2,3,-Dioxygenase Inflammation/immunology Macrophages/*immunology/*microbiology Nitric Oxide/metabolism Oxidoreductases/metabolism Respiratory Burst Tryptophan Oxygenase/metabolism Tumor Necrosis Factor-alpha/metabolism
Pubmed
Web of science
Création de la notice
25/01/2008 15:27
Dernière modification de la notice
20/08/2019 16:13
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