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1.
Eur J Pharmacol ; 981: 176856, 2024 Oct 15.
Artículo en Inglés | MEDLINE | ID: mdl-39068979

RESUMEN

Autophagy is a fundamental pillar of cellular resilience, indispensable for maintaining cellular health and vitality. It coordinates the meticulous breakdown of cytoplasmic macromolecules as a guardian of cell metabolism, genomic integrity, and survival. In the complex play of biological warfare, autophagy emerges as a firm defender, bravely confronting various pathogenic, infectious, and cancerous adversaries. Nevertheless, its role transcends mere defense, wielding both protective and harmful effects in the complex landscape of disease pathogenesis. From the onslaught of infectious outbreaks to the devious progression of chronic lifestyle disorders, autophagy emerges as a central protagonist, convolutedly shaping the trajectory of cellular health and disease progression. In this article, we embark on a journey into the complicated web of molecular and immunological mechanisms that govern autophagy's profound influence over disease. Our focus sharpens on dissecting the impact of various autophagy-associated proteins on the kaleidoscope of immune responses, spanning the spectrum from infectious outbreaks to chronic lifestyle ailments. Through this voyage of discovery, we unveil the vast potential of autophagy as a therapeutic linchpin, offering tantalizing prospects for targeted interventions and innovative treatment modalities that promise to transform the landscape of disease management.


Asunto(s)
Autofagia , Humanos , Animales
2.
Eur J Pharmacol ; 975: 176637, 2024 Jul 15.
Artículo en Inglés | MEDLINE | ID: mdl-38729416

RESUMEN

Macrophages play a pivotal role in safeguarding against a broad spectrum of infections, from viral, bacterial, fungal to parasitic threats and contributing to the immune defense against cancer. While morphine's immunosuppressive effects on immune cells are extensively documented, a significant knowledge gap exists regarding its influence on macrophage polarization and differentiation. Hence, we conducted a study that unveils that prior exposure to morphine significantly impedes the differentiation of bone marrow cells into macrophages. Furthermore, the polarization of macrophages toward the M1 phenotype under M1-inducing conditions experiences substantial impairment, as evidenced by the diminished expression of CD80, CD86, CD40, iNOS, and MHCII. This correlates with reduced expression of M1 phenotypical markers such as iNOS, IL-1ß, and IL-6, accompanied by noticeable morphological, size, and phagocytic alterations. Further, we also observed that morphine affected M2 macrophages. These findings emphasize the necessity for a more comprehensive understanding of the impact of morphine on compromising macrophage function and its potential ramifications for therapeutic approaches.


Asunto(s)
Diferenciación Celular , Inmunosupresores , Macrófagos , Morfina , Morfina/farmacología , Animales , Macrófagos/efectos de los fármacos , Macrófagos/inmunología , Ratones , Diferenciación Celular/efectos de los fármacos , Inmunosupresores/farmacología , Polaridad Celular/efectos de los fármacos , Óxido Nítrico Sintasa de Tipo II/metabolismo , Ratones Endogámicos C57BL , Fagocitosis/efectos de los fármacos , Activación de Macrófagos/efectos de los fármacos , Masculino , Interleucina-1beta/metabolismo
3.
J Biol Chem ; 298(12): 102596, 2022 12.
Artículo en Inglés | MEDLINE | ID: mdl-36257405

RESUMEN

Novel vaccination strategies are crucial to efficiently control tuberculosis, as proposed by the World Health Organization under its flagship program "End TB Strategy." However, the emergence of drug-resistant strains of Mycobacterium tuberculosis (Mtb), particularly in those coinfected with HIV-AIDS, constitutes a major impediment to achieving this goal. We report here a novel vaccination strategy that involves synthesizing a formulation of an immunodominant peptide derived from the Acr1 protein of Mtb. This nanoformulation in addition displayed on the surface a toll-like receptor-2 ligand to offer to target dendritic cells (DCs). Our results showed an efficient uptake of such a concoction by DCs in a predominantly toll-like receptor-2-dependent pathway. These DCs produced elevated levels of nitric oxide, proinflammatory cytokines interleukin-6, interleukin-12, and tumor necrosis factor-α, and upregulated the surface expression of major histocompatibility complex class II molecules as well as costimulatory molecules such as CD80 and CD86. Animals injected with such a vaccine mounted a significantly higher response of effector and memory Th1 cells and Th17 cells. Furthermore, we noticed a reduction in the bacterial load in the lungs of animals challenged with aerosolized live Mtb. Therefore, our findings indicated that the described vaccine triggered protective anti-Mtb immunity to control the tuberculosis infection.


Asunto(s)
Mycobacterium tuberculosis , Tuberculosis , Animales , Células Dendríticas , Epítopos , Ligandos , Mycobacterium tuberculosis/metabolismo , Receptor Toll-Like 2/metabolismo , Tuberculosis/prevención & control , Tuberculosis/microbiología , Ratones
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