Resistance to Prostaglandin E2 Promotes Monocyte Activation During Chronic HIV Infection.

Autor:	Di Diego Garcia F; Instituto de Investigaciones Biomdicas en Retrovirus y SIDA, Universidad de Buenos Aires/CONICET, Buenos Aires, Argentina., Cabrerizo G; Instituto de Investigaciones Biomdicas en Retrovirus y SIDA, Universidad de Buenos Aires/CONICET, Buenos Aires, Argentina., Paletta A; Instituto de Investigaciones Biomdicas en Retrovirus y SIDA, Universidad de Buenos Aires/CONICET, Buenos Aires, Argentina., Prez PS; Instituto de Investigaciones Biomdicas en Retrovirus y SIDA, Universidad de Buenos Aires/CONICET, Buenos Aires, Argentina., Varese A; Instituto de Investigaciones Biomdicas en Retrovirus y SIDA, Universidad de Buenos Aires/CONICET, Buenos Aires, Argentina., Geffner J; Instituto de Investigaciones Biomdicas en Retrovirus y SIDA, Universidad de Buenos Aires/CONICET, Buenos Aires, Argentina., Bello N; Divisin Infectologa, Hospital de Clnicas Jos de San Martn, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina., Fridman V; Divisin Infectologa, Hospital de Clnicas Jos de San Martn, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina., Stecher D; Divisin Infectologa, Hospital de Clnicas Jos de San Martn, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina., Ceballos A; Instituto de Investigaciones Biomdicas en Retrovirus y SIDA, Universidad de Buenos Aires/CONICET, Buenos Aires, Argentina., Remes Lenicov F; Instituto de Investigaciones Biomdicas en Retrovirus y SIDA, Universidad de Buenos Aires/CONICET, Buenos Aires, Argentina.
Jazyk:	angličtina
Zdroj:	The Journal of infectious diseases [J Infect Dis] 2023 Feb 01; Vol. 227 (3), pp. 423-433.
DOI:	10.1093/infdis/jiac480
Abstrakt:	Background: Monocyte activation is a driver of inflammation in the course of chronic HIV infection. Prostaglandin E2 (PGE2) is known to mediate anti-inflammatory effects, notably the inhibition of tumor necrosis factor- (TNF-) production by monocytes. We aim to investigate the effects of PGE2 on activation of monocytes in chronic HIV infection and the mechanisms through which PGE2 modulates their inflammatory signature. Methods: We recruited a group of people with HIV (PWH) and matched healthy uninfected persons. We compared plasma levels of PGE2, monocyte activation, and sensitivity of monocytes to the inhibitory actions mediated by PGE2. Results: We found increased plasma levels of PGE2 in PWH, and an activated phenotype in circulating monocytes, compared with uninfected individuals. Monocytes from PWH showed a significant resistance to the inhibitory actions mediated by PGE2; the concentration of PGE2 able to inhibit 50 of the production of TNF- by lipopolysaccharide-stimulated monocytes was 10 times higher in PWH compared with uninfected controls. Furthermore, the expression of phosphodiesterase 4B, a negative regulator of PGE2 activity, was significantly increased in monocytes from PWH. Conclusions: Resistance to the inhibitory actions mediated by PGE2 could account, at least in part, for the inflammatory profile of circulating monocytes in PWH. (The Author(s) 2022. Published by Oxford University Press on behalf of Infectious Diseases Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)
Databáze:	MEDLINE
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