Infectious diseases of different etiologies have been associated with acute and long-term neurological consequences. The primary cause of these consequences appears to be an inflammatory process characterized primarily by a pro-inflammatory microglial state. Microglial cells, the local effectors' cells of innate immunity, once faced by a stimulus, alter their morphology, and become a primary source of inflammatory cytokines that increase the inflammatory process of the brain. This inflammatory scenario exerts a critical role in the pathogenesis of neurodegenerative diseases. In recent years, several studies have shown the involvement of the microglial inflammatory response caused by infections in the development of neurodegenerative diseases. This has been associated with a transitory microglial state subsequent to an inflammatory response, known as microglial priming, in which these cells are more responsive to stimuli. Thus, systemic inflammation and infections induce a transitory state in microglia that may lead to changes in their state and function, making priming them for subsequent immune challenges. However, considering that microglia are long-lived cells and are repeatedly exposed to infections during a lifetime, microglial priming may not be beneficial. In this review, we discuss the relationship between infections and neurodegenerative diseases and how this may rely on microglial priming.
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http://dx.doi.org/10.3389/fncel.2022.878987 | DOI Listing |
Int J Mol Sci
December 2024
Department of Anatomy, "Carol Davila" University of Medicine and Pharmacy, 050474 Bucharest, Romania.
Neuroimmunology is reshaping the understanding of the central nervous system (CNS), revealing it as an active immune organ rather than an isolated structure. This review delves into the unprecedented discoveries transforming the field, including the emerging roles of microglia, astrocytes, and the blood-brain barrier (BBB) in orchestrating neuroimmune dynamics. Highlighting their dual roles in both repair and disease progression, we uncover how these elements contribute to the intricate pathophysiology of neurodegenerative diseases, cerebrovascular conditions, and CNS tumors.
View Article and Find Full Text PDFEur Arch Psychiatry Clin Neurosci
December 2024
Laboratory of Clinical Neuropathology, Mental Health Research Center, Kashirskoe Shosse 34, 115522, Moscow, Russia.
Previously we found altered microglia-neuron interactions in the prefrontal cortex in schizophrenia. We hypothesized that microglia-neuron interactions may be dysregulated in the caudate nucleus in schizophrenia. A postmortem ultrastructural morphometric study was performed to investigate satellite microglia (SatMg) and adjacent neurons in the head of the caudate nucleus in 21 cases of schizophrenia and 20 healthy controls.
View Article and Find Full Text PDFGlia
December 2024
Molecular and Cellular Pharmacology Program, Stony Brook, New York, USA.
Chronic stress is a major contributor to the development of major depressive disorder, one of the leading causes of disability worldwide. Using a model of repeated social defeat stress in mice, we and others have reported that neuroinflammation plays a dynamic role in the development of behavioral deficits consistent with social avoidance and impaired reward responses. Animals susceptible to the model also exhibit hypomyelination in the medial prefrontal cortex, indicative of changes in the differentiation pathway of cells of the oligodendroglial lineage (OLN).
View Article and Find Full Text PDFBrain Behav Immun
December 2024
Department of Integrative Physiology, University of Colorado Boulder, Boulder, CO 80309, USA; Department of Psychology and Neuroscience, University of Colorado Boulder, Boulder, CO 80309, USA; Center for Microbial Exploration, University of Colorado Boulder, Boulder, CO 80309, USA; Center for Neuroscience, University of Colorado Boulder, Boulder, CO 80309, USA; Department of Physical Medicine and Rehabilitation and Center for Neuroscience, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA. Electronic address:
The prevalence of noncommunicable inflammatory disease is increasing in modern urban societies, posing significant challenges to public health. Novel prevention and therapeutic strategies are needed to effectively deal with this issue. One promising approach is leveraging microorganisms such as Mycobacterium vaccae ATCC 15483, known for its anti-inflammatory, immunoregulatory, and stress-resilience properties.
View Article and Find Full Text PDFBiomed Res Int
December 2024
Department of Life Science, Gachon University, Seongnam, Gyeonggi-do 13120, Republic of Korea.
Innate immune memory or trained immunity refers to a long-lasting response of the innate immune cells against repeated exposure to the homogenous or heterogenous infectious agent. The trained immunity is induced through epigenetic modification and is characterized by the change of both intracellular immunological signaling and cellular metabolism. Recently, different groups have tried to establish protocols to generate trained innate immune cells.
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