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Spotlights on immunological effects of reactive nitrogen species: When inflammation says nitric oxide

World Journal of Experimental Medicine 2015年第2期5卷 64-76页

作者： Andrea Predonzani Bianca Calì andrielly HR agnellini Barbara Molon Veneto Institute of Oncology IOV IRCCS Venetian Institute of Molecular Medicine Department of Biomedical Sciences University of Padua Department of Surgery Oncology and Gastroenterology Oncology and Immunology Section University of Padua

Over the last decades, nitric oxide(NO) has been definitively recognised as one of the key players involved in immunity and inflammation. NO generation was originally described in activated macrophages, which still represent the prototype of NO-producing cells. Notwithstanding, additional cell subsets belonging to both innate and adaptive immunity have been documented to sustain NO propagation by means of the enzymatic activity of different nitric oxide synthase isoforms. Furthermore, due to its chemical characteristics, NO could rapidly react with other free radicals to generate different reactive nitrogen species(RNS), which have been intriguingly associated with many pathological conditions. Nonetheless, the plethora of NO/RNS-mediated effects still remains extremely puzzling. The aim of this manuscript is to dig into the broad literature on the topic to provide intriguing insights on NO-mediated circuits within immune system. We analysed NO and RNS immunological clues arising from their biochemical properties, immunomodulatory activities and finally dealing with their impact on different pathological scenarios with far prompting intriguing perspectives for their pharmacological targeting.

关键词： Nitric oxide Reactive nitrogen species Post-translational modification Immune cells Immune diseases

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Targeting monoamine oxidase to dampen NLRP3 inflammasome activation in inflammation

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Cellular & Molecular Immunology 2021年第5期18卷 1311-1313页

作者： Ricardo Sánchez-Rodríguez Fabio Munari Roberta Angioni Francisca Venegas andrielly agnellini María Paulette Castro-Gil Alessandra Castegna Roberto Luisetto Antonella Viola Marcella Canton Department of Biomedical Sciences University of Padova35131PadovaItaly Fondazione Istituto di Ricerca Pediatrica Cittàdella Speranza-IRP 35129PadovaItaly Venetian Institute of Molecular Medicine PadovaItaly Laboratorio de Enfermedades Hepáticas Instituto Nacional de Medicina GenómicaCDMXMexico Department of Biosciences Biotechnologies and BiopharmaceuticsUniversity of BariBariItaly Department of Surgery Oncology and GastroenterologyUniversity of PadovaPadovaItaly

Inflammasomes represent protective weapons against pathogens and cellular damage,although their uncontrolled activation drives the progression of inflammatory,metabolic,and neurodegenerative *** signals activate the NLRP3 inflammasome,and a few studies have reported that mitochondrial reactive oxygen species(ROS)are involved in this ***,the source of mitochondrial ROS and their specific role in NLRP3 triggering are ***,we show that H2O2 produced by the mitochondrial enzyme monoamine oxidase B(MAO-B)plays a nonredundant role in sustaining NLRP3 inflammasome ***,MAO-B-dependent ROS formation caused mitochondrial dysfunction and NF-κB induction,resulting in NLRP3 and pro-IL-1β*** in vitro and in vivo,MAO-B inhibition by rasagiline prevented IL-1βsecretion,and MAO-B-deficient mice showed an impaired response to LPS-mediated *** findings identify MAO-B as a specific producer of mitochondrial ROS fueling the NLRP3 inflammasome,thereby providing a basis for repurposing MAOB inhibitors to treat inflammasome-mediated pathologies.

关键词： NLRP3 inflam impaired

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