Abstract
Mitochondria are the energy center of the cell. They are found in the cell cytoplasm as dynamic networks where they adapt energy production based on the cell’s needs. They are also at the center of the proinflammatory response and have essential roles in the response against pathogenic infections. Mitochondria are a major site for production of Reactive Oxygen Species (ROS; or free radicals), which are essential to fight infection. However, excessive and uncontrolled production can become deleterious to the cell, leading to mitochondrial and tissue damage. Pathogens exploit the role of mitochondria during infection by affecting the oxidative phosphorylation mechanism (OXPHOS), mitochondrial network and disrupting the communication between the nucleus and the mitochondria. The role of mitochondria in these biological processes makes these organelle good targets for the development of therapeutic strategies. In this review, we presented a summary of the endosymbiotic origin of mitochondria and their involvement in the pathogen response, as well as the potential promising mitochondrial targets for the fight against infectious diseases and chronic inflammatory diseases.
Highlights
Fission is mediated by dynamin-related protein 1 (DRP1), which is recruited from the cytosol to form spirals around mitochondria that constrict to sever both inner and outer membranes
Fusion between mitochondrial outer membranes is mediated by membrane-anchored dynamin family members named mitofusins MFN1 and MFN2, whereas fusion between mitochondrial inner membranes is mediated by a single dynamin family member called OPA1 mitochondrial dynamin-like guanosine triphosphatases (GTPases) (OPA1) in mammals
Infection with Epstein-Barr virus (EBV), an oncovirus associated with Burkitt lymphoma, reduces mitochondria content in differentiating monocytes [109], remodels B cell mitochondria by targeting the mitochondrial 1-Carbon pathway involved in the synthesis of purine, thymidylate and glutathione [110] and induces mitochondria swelling, cyclophilin D dependent mitochondrial membrane permeabilization transition (MMPT), decreased mitochondrial membrane potential (∆ψm) and ATP, increased Reactive Oxygen Species (ROS) production and mitophagy and reduced apoptosis [111]
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. The eukaryotic cell is defined essentially by the existence of a structured nucleus and the presence of organelles in the cytoplasm such as mitochondria in contrast to prokaryotes. In the course of evolution, the ancestral mitochondria and the host have each set up weapons to eliminate the other It is the co-evolution of these two organisms that has allowed creating the programmed cell death mechanism as we know today [21]. By increasing energy production [25], the ancestral cell was able to extend its genome and to allow an increase in cellular complexity [26] This increased energy allowed the eukaryotic cell to set up several mechanisms such as the cell cycle, endomembrane traffic [26], the nucleus compartmentalization [27] and the ability to become multicellular
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