About this Research Topic
Accumulating evidence supports the role of infections in the etiopathogenesis of inflammatory disorders of the central nervous system, including multiple sclerosis, neuromyelitis optica spectrum disorders, and myelin oligodendrocyte glycoprotein antibody-associated disease; however, the mechanism underlying this association remains unclear. Mitochondria play a critical role during the proinflammatory response against pathogenic infections, and neuroinflammation-related mitochondrial dysfunction occurs in several neuroinflammatory and neurodegenerative disorders.
Dysfunctional mitochondria can trigger the production of reactive oxygen species and activate inflammatory pathway, leading to chronic inflammation. This chronic inflammation can have detrimental effects on neurons, glial cells, and immune cells, contributing to immune system dysregulation and neurodegeneration.
The imbalanced activity of mitochondria is involved in inflammation and dysfunctional response to infection. For example, proteins encoded by Epstein-Barr virus, both during the latency and lytic infection, reduce autophagy, decrease intracellular reactive oxygen species, and modulate mitochondrial function, altering bioenergetics. Bacterial proteins can act as virulence factors by modulating mitochondrial physiology for bacterial survival and immune evasion within host cells, inducing macrophage apoptosis via a mitochondrial pathway in macrophages.
So far, very little is known about the cellular and molecular mechanisms of mitochondrial functions in response to pathogens when inflammation occurs in the brain, or how infections might alter the mitochondrial homeostasis in innate cells by influencing the host’s innate inflammatory response. Therefore, this research topic intends to focus on the complex link between mitochondrial dysfunction, infection, and neuroinflammation. We will accumulate evidence on the underlying mechanisms involved in the pathogenesis and progression of neuroinflammatory disorders, shed new light on the crosstalk between microbes and mitochondria during neuroinflammation, dissect the contribution of different genes and pathogens, and consequently provide a possibility for novel neuroprotective therapies.
In this research topic, we welcome contributions in the form of original research, review, mini review, and hypothesis and theory articles focusing on, but not limited to, the following themes:
• The link between neuronal mitophagy and infection
• Detection of markers of mitophagy in patients with neurological disorders
• Relationship between risk of infection, mitochondrial dysfunction, and treatment
• The interplay between mitochondria and infection in animal model systems of neurological diseases
• Detailed mechanistic studies for enhancing our understanding of the interplay of mitochondrial function and the immune system
Dysfunctional mitochondria can trigger the production of reactive oxygen species and activate inflammatory pathway, leading to chronic inflammation. This chronic inflammation can have detrimental effects on neurons, glial cells, and immune cells, contributing to immune system dysregulation and neurodegeneration.
The imbalanced activity of mitochondria is involved in inflammation and dysfunctional response to infection. For example, proteins encoded by Epstein-Barr virus, both during the latency and lytic infection, reduce autophagy, decrease intracellular reactive oxygen species, and modulate mitochondrial function, altering bioenergetics. Bacterial proteins can act as virulence factors by modulating mitochondrial physiology for bacterial survival and immune evasion within host cells, inducing macrophage apoptosis via a mitochondrial pathway in macrophages.
So far, very little is known about the cellular and molecular mechanisms of mitochondrial functions in response to pathogens when inflammation occurs in the brain, or how infections might alter the mitochondrial homeostasis in innate cells by influencing the host’s innate inflammatory response. Therefore, this research topic intends to focus on the complex link between mitochondrial dysfunction, infection, and neuroinflammation. We will accumulate evidence on the underlying mechanisms involved in the pathogenesis and progression of neuroinflammatory disorders, shed new light on the crosstalk between microbes and mitochondria during neuroinflammation, dissect the contribution of different genes and pathogens, and consequently provide a possibility for novel neuroprotective therapies.
In this research topic, we welcome contributions in the form of original research, review, mini review, and hypothesis and theory articles focusing on, but not limited to, the following themes:
• The link between neuronal mitophagy and infection
• Detection of markers of mitophagy in patients with neurological disorders
• Relationship between risk of infection, mitochondrial dysfunction, and treatment
• The interplay between mitochondria and infection in animal model systems of neurological diseases
• Detailed mechanistic studies for enhancing our understanding of the interplay of mitochondrial function and the immune system
Keywords: multiple sclerosis, NMOSD, MOGAD, mitochondria, infection
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
