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Lack of microbicidal response in human macrophages infected with Parachlamydia acanthamoebae

Abstract : 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.
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https://hal-amu.archives-ouvertes.fr/hal-02025873
Contributor : Benoit Desnues <>
Submitted on : Tuesday, February 19, 2019 - 9:58:32 PM
Last modification on : Monday, February 17, 2020 - 9:34:03 AM

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Gilbert Greub, Benoit Desnues, Didier Raoult, Jean-Louis Mege. Lack of microbicidal response in human macrophages infected with Parachlamydia acanthamoebae. Microbes and Infection, Elsevier, 2005, 7 (4), pp.714-719. ⟨10.1016/j.micinf.2005.01.009⟩. ⟨hal-02025873⟩

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