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- W4313385237 abstract "Abstract Autophagy and cytokine response are both involved in host defense against intracellular bacteria, including Brucella. However the effect of autophagy on the balance of Brucella triggered pro- and anti-inflammatory cytokine production has not been studied in the human system. In the present study, we assessed the effect of autophagy on pro- and anti-inflammatory cytokine production, using primary human monocytes infected with live clinical strain of B. melitensis in the presence or absence of specific autophagy inhibitors (Wortmannin, LY294002). Autophagy inhibition resulted in significant induction mainly of IL-1b and TNF-a release as detected at the cell culture supernatants after 16h of stimulation. The effect was less prominent on IL-6 production. Most importantly IL-10 production was drastically reduced in the presence of autophagy inhibitors. Activation of specific autophagy proteins in THP-1 cells infected with B. melitensis was detected at different time points of infection. Differentiation of THP-1 cells to macrophage phenotype induced autophagy as detected by the formation of LC3II complex. Prolonged stimulation with B. melitensis (2–24h) neither altered the formation of LC3II complex nor affected the amount of ULK1 protein. Microarray analysis of the transcriptional response of peripheral human monocytes 4h postinfection with B. melitensis, revealed a dramatic increase of a protein upstream of LC3II that has an essential role in regulation of autophagy. These results suggest that autophagy differentially regulates cytokine response against B. melitensis in humans, modulating inflammation probably by interfering in signaling pathways initiated by key autophagy proteins." @default.
- W4313385237 created "2023-01-06" @default.
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- W4313385237 date "2017-05-01" @default.
- W4313385237 modified "2023-09-27" @default.
- W4313385237 title "<i>Brucella melitensis</i> specifically interferes with autophagy pathway in human monocytes and enhances anti-inflammatory response." @default.
- W4313385237 doi "https://doi.org/10.4049/jimmunol.198.supp.77.24" @default.
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