PGE2 displays immunosuppressive effects during human active tuberculosis

Abstract Prostaglandin E2 (PGE2), an active lipid compound derived from arachidonic acid, regulates different stages of the immune response of the host during several pathologies such as chronic infections or cancer. In fact, manipulation of PGE2 levels was proposed as an approach for countering the...

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Autores principales:	Joaquín Miguel Pellegrini, Candela Martin, María Paula Morelli, Julieta Aylen Schander, Nancy Liliana Tateosian, Nicolás Oscar Amiano, Agustín Rollandelli, Domingo Juan Palmero, Alberto Levi, Lorena Ciallella, María Isabel Colombo, Verónica Edith García
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/e3730db0604c4b0fb9b9154b50e38f08
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spelling	oai:doaj.org-article:e3730db0604c4b0fb9b9154b50e38f082021-12-02T14:33:51ZPGE2 displays immunosuppressive effects during human active tuberculosis10.1038/s41598-021-92667-12045-2322https://doaj.org/article/e3730db0604c4b0fb9b9154b50e38f082021-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-92667-1https://doaj.org/toc/2045-2322Abstract Prostaglandin E2 (PGE2), an active lipid compound derived from arachidonic acid, regulates different stages of the immune response of the host during several pathologies such as chronic infections or cancer. In fact, manipulation of PGE2 levels was proposed as an approach for countering the Type I IFN signature of tuberculosis (TB). However, very limited information regarding the PGE2 pathway in patients with active TB is currently available. In the present work, we demonstrated that PGE2 exerts a potent immunosuppressive action during the immune response of the human host against Mycobacterium tuberculosis (Mtb) infection. Actually, we showed that PGE2 significantly reduced the surface expression of several immunological receptors, the lymphoproliferation and the production of proinflammatory cytokines. In addition, PGE2 promoted autophagy in monocytes and neutrophils cultured with Mtb antigens. These results suggest that PGE2 might be attenuating the excessive inflammatory immune response caused by Mtb, emerging as an attractive therapeutic target. Taken together, our findings contribute to the knowledge of the role of PGE2 in the human host resistance to Mtb and highlight the potential of this lipid mediator as a tool to improve anti-TB treatment.Joaquín Miguel PellegriniCandela MartinMaría Paula MorelliJulieta Aylen SchanderNancy Liliana TateosianNicolás Oscar AmianoAgustín RollandelliDomingo Juan PalmeroAlberto LeviLorena CiallellaMaría Isabel ColomboVerónica Edith GarcíaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-14 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Joaquín Miguel Pellegrini Candela Martin María Paula Morelli Julieta Aylen Schander Nancy Liliana Tateosian Nicolás Oscar Amiano Agustín Rollandelli Domingo Juan Palmero Alberto Levi Lorena Ciallella María Isabel Colombo Verónica Edith García PGE2 displays immunosuppressive effects during human active tuberculosis
description	Abstract Prostaglandin E2 (PGE2), an active lipid compound derived from arachidonic acid, regulates different stages of the immune response of the host during several pathologies such as chronic infections or cancer. In fact, manipulation of PGE2 levels was proposed as an approach for countering the Type I IFN signature of tuberculosis (TB). However, very limited information regarding the PGE2 pathway in patients with active TB is currently available. In the present work, we demonstrated that PGE2 exerts a potent immunosuppressive action during the immune response of the human host against Mycobacterium tuberculosis (Mtb) infection. Actually, we showed that PGE2 significantly reduced the surface expression of several immunological receptors, the lymphoproliferation and the production of proinflammatory cytokines. In addition, PGE2 promoted autophagy in monocytes and neutrophils cultured with Mtb antigens. These results suggest that PGE2 might be attenuating the excessive inflammatory immune response caused by Mtb, emerging as an attractive therapeutic target. Taken together, our findings contribute to the knowledge of the role of PGE2 in the human host resistance to Mtb and highlight the potential of this lipid mediator as a tool to improve anti-TB treatment.
format	article
author	Joaquín Miguel Pellegrini Candela Martin María Paula Morelli Julieta Aylen Schander Nancy Liliana Tateosian Nicolás Oscar Amiano Agustín Rollandelli Domingo Juan Palmero Alberto Levi Lorena Ciallella María Isabel Colombo Verónica Edith García
author_facet	Joaquín Miguel Pellegrini Candela Martin María Paula Morelli Julieta Aylen Schander Nancy Liliana Tateosian Nicolás Oscar Amiano Agustín Rollandelli Domingo Juan Palmero Alberto Levi Lorena Ciallella María Isabel Colombo Verónica Edith García
author_sort	Joaquín Miguel Pellegrini
title	PGE2 displays immunosuppressive effects during human active tuberculosis
title_short	PGE2 displays immunosuppressive effects during human active tuberculosis
title_full	PGE2 displays immunosuppressive effects during human active tuberculosis
title_fullStr	PGE2 displays immunosuppressive effects during human active tuberculosis
title_full_unstemmed	PGE2 displays immunosuppressive effects during human active tuberculosis
title_sort	pge2 displays immunosuppressive effects during human active tuberculosis
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/e3730db0604c4b0fb9b9154b50e38f08
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PGE2 displays immunosuppressive effects during human active tuberculosis

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