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Host-Derived Lipids from Tuberculous Pleurisy Impair Macrophage Microbicidal-Associated Metabolic Activity. 2020
José Luis Marín Franco, and
Melanie Genoula, and
Dan Corral, and
Gabriel Duette, and
Malena Ferreyra, and
Mariano Maio, and
María Belén Dolotowicz, and
Omar Emiliano Aparicio-Trejo, and
Eduardo Patiño-Martínez, and
Alison Charton, and
Arnaud Métais, and
Federico Fuentes, and
Vanessa Soldan, and
Eduardo José Moraña, and
Domingo Palmero, and
Matías Ostrowski, and
Pablo Schierloh, and
Carmen Sánchez-Torres, and
Rogelio Hernández-Pando, and
José Pedraza-Chaverri, and
Yoann Rombouts, and
Denis Hudrisier, and
Emilie Layre, and
Christel Vérollet, and
Isabelle Maridonneau-Parini, and
Olivier Neyrolles, and
María Del Carmen Sasiain, and
Geanncarlo Lugo-Villarino, and
Luciana Balboa
Instituto de Medicina Experimental (IMEX)-CONICET, Academia Nacional de Medicina, Buenos Aires C1425ASU, Argentina; International Associated Laboratory (LIA) CNRS IM-TB/HIV (1167), Buenos Aires, Argentina - Toulouse, France.
Mycobacterium tuberculosis (Mtb) regulates the macrophage metabolic state to thrive in the host, yet the responsible mechanisms remain elusive. Macrophage activation toward the microbicidal (M1) program depends on the HIF-1α-mediated metabolic shift from oxidative phosphorylation (OXPHOS) toward glycolysis. Here, we ask whether a tuberculosis (TB) microenvironment changes the M1 macrophage metabolic state. We expose M1 macrophages to the acellular fraction of tuberculous pleural effusions (TB-PEs) and find lower glycolytic activity, accompanied by elevated levels of OXPHOS and bacillary load, compared to controls. The eicosanoid fraction of TB-PE drives these metabolic alterations. HIF-1α stabilization reverts the effect of TB-PE by restoring M1 metabolism. Furthermore, Mtb-infected mice with stabilized HIF-1α display lower bacillary loads and a pronounced M1-like metabolic profile in alveolar macrophages (AMs). Collectively, we demonstrate that lipids from a TB-associated microenvironment alter the M1 macrophage metabolic reprogramming by hampering HIF-1α functions, thereby impairing control of Mtb infection.
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