Neuroimmune crosstalk in chronic neuroinflammation: microglial interactions and immune modulation DOI Creative Commons

Ludmila Müller,

Svetlana Di Benedetto

Frontiers in Cellular Neuroscience, Год журнала: 2025, Номер 19

Опубликована: Апрель 7, 2025

Neuroinflammation is a fundamental feature of many chronic neurodegenerative diseases, where it contributes to disease onset, progression, and severity. This persistent inflammatory state arises from the activation innate adaptive immune responses within central nervous system (CNS), orchestrated by complex interplay resident cells, infiltrating peripheral an array molecular mediators such as cytokines, chemokines, extracellular vesicles. Among CNS-resident microglia play role, exhibiting dynamic spectrum phenotypes ranging neuroprotective neurotoxic. In sustained microglial often leads amplification cascades, reinforcing pathogenic cycle immune-mediated damage. Intercellular communication inflamed CNS persistence progression neuroinflammation. Microglia engage in extensive crosstalk with astrocytes, neurons, oligodendrocytes, shaping both local systemic responses. These interactions influence key processes synaptic pruning, phagocytosis, blood–brain barrier integrity, cytokine-mediated signaling. Understanding mechanisms cell–cell signaling this context critical for identifying therapeutic strategies modulate response restore homeostasis. review explores players neuroinflammation, focus on role microglia, pathways underlying intercellular communication, potential approaches mitigate neuroinflammatory damage diseases.

Язык: Английский

Editorial: Glial cells in health and disease: impacts on neural circuits and plasticity DOI Creative Commons
Shirin Hosseini, Poonam Thakur, David L. Cedeño

и другие.

Frontiers in Cellular Neuroscience, Год журнала: 2025, Номер 19

Опубликована: Фев. 20, 2025

This research topic has markedly enhanced the current understanding of role glial cells on pathological conditions both central nervous system (CNS) and peripheral (PNS) (Verkhratsky et al., 2014; Tan al. 2021). The diversity these is largely dictated by in particular regions affected neural tissue distinct interactions other cells. Investigating common molecular mechanisms underlying can illuminate pathways for developing innovative therapeutic strategies.This comprehensive analysis synthesizes findings from pivotal studies this topic, highlighting critical intersections between neuroimmunology cellular neurophysiology. study Kleidonas delineates acute effects elevated ammonia levels, relevant to liver dysfunction, synaptic transmission CA1 neurons mouse entorhino-hippocampus tissue. Elevated suppresses neuronal action due their impact astrocyte functionality, key regulatory that astrocytes play maintaining homeostasis, through modulating excitatory synapses. Importantly, it was observed inhibition glutamine synthetase, an astrocytic enzyme, mitigates downregulation transmissions, reinforcing function.Concurrently, Gabele delves into sex-specific neurotropic influenza A virus (H7N7 strain) hippocampal It unveils female-derived exhibit a more pronounced innate immune response, marked interferon-β chemokine secretion, leading differential microglial activation morphological changes compared male-derived variation response highlights intricate dynamics pathogen or stressor-host within CNS, which warrants careful consideration effect future endeavors (Chen 2018).The review Kveštak extends discussion Innate Lymphoid Cells (ILCs), which, although minor component CNS under physiological conditions, infiltrate parenchyma during neuroinflammatory infectious scenarios. ILCs, with cells, including microglia, modulate responses, thereby influencing outcomes autoimmune diseases viral infections. ILC function aligns previous two suggesting potential synergistic stress responses modulation CNS.The PNS alongside those (Müller 2025). Mohamed enhances our multifaceted roles protein kinase C epsilon type (PKCε) PNS. While PKCε already recognized its involvement cancer progression, uncovers novel Schwann (SCs), PNS, are crucial nerve regeneration functionality. work elucidates capacity SCs proliferation, migration, differentiation, facilitating transition proliferative differentiated states, as well epithelial-mesenchymal transition-like process. identification BDNF-TrkB-PKCε autocrine signaling axis provides valuable insights regulating plasticity. groundbreaking suggests targeting pathway may open new avenues addressing injuries, neuropathic pain, tumors, related neuropathies, broadening scope intervention PNS-related disorders.In conducted Schröder rational drug design approach employed address Multiple Sclerosis (MS), chronic, autoimmune, demyelinating disease CNS; clinical have demonstrated subgroup patients (Adamec focused polysialic acid (polySia), glycan immunomodulatory properties, demonstrating benefits upregulation myelin. Notably, application polySia chain length DP24–30 organotypic murine brain slices found significantly enhance remyelination. mediated via inhibitory receptor Siglec-E. Furthermore, indicate effectively reduces proinflammatory fostering environment supports myelin regeneration. By elucidating pro-regenerative capabilities polySia, contributes deeper repair, establishing promising target treating such MS.Remarkably, investigation particularly intriguing, been shown proliferation promoting myelination, could offer injuries.In mini-review Gjervan alternative strategy repair presented, focusing claudin-11, tight junctions sheath. Recent elucidated heterozygous stop-loss mutations CLDN11 gene implicated etiology hypomyelinating leukodystrophy 22 (HLD22), genetic disorder characterized impaired myelination. Investigations claudin-11-deficient models significant impairments, delayed transmission, auditory deficits, male sterility, revealing protein. These underscore urgency further aimed at full spectrum claudin-11's functions advancing development effective interventions, not only HLD22 but also diseases.Together, articles nuanced paradigm where interact differentially metabolic, pathologic stressors, influenced inherent sex-based immunological differences (Figure 1). integrative perspective advances pathophysiology, regulation, cell interactions, interventions disorders context chronic conditions.

Язык: Английский

Процитировано

0
Cognitive Frailty: A Comprehensive Clinical Paradigm Beyond Cognitive Decline DOI
Mariagiovanna Cozza, Virginia Boccardi

Ageing Research Reviews, Год журнала: 2025, Номер unknown, С. 102738 - 102738

Опубликована: Март 1, 2025

Язык: Английский

Процитировано

0
Neuroimmune crosstalk in chronic neuroinflammation: microglial interactions and immune modulation DOI Creative Commons

Ludmila Müller,

Svetlana Di Benedetto

Frontiers in Cellular Neuroscience, Год журнала: 2025, Номер 19

Опубликована: Апрель 7, 2025

Neuroinflammation is a fundamental feature of many chronic neurodegenerative diseases, where it contributes to disease onset, progression, and severity. This persistent inflammatory state arises from the activation innate adaptive immune responses within central nervous system (CNS), orchestrated by complex interplay resident cells, infiltrating peripheral an array molecular mediators such as cytokines, chemokines, extracellular vesicles. Among CNS-resident microglia play role, exhibiting dynamic spectrum phenotypes ranging neuroprotective neurotoxic. In sustained microglial often leads amplification cascades, reinforcing pathogenic cycle immune-mediated damage. Intercellular communication inflamed CNS persistence progression neuroinflammation. Microglia engage in extensive crosstalk with astrocytes, neurons, oligodendrocytes, shaping both local systemic responses. These interactions influence key processes synaptic pruning, phagocytosis, blood–brain barrier integrity, cytokine-mediated signaling. Understanding mechanisms cell–cell signaling this context critical for identifying therapeutic strategies modulate response restore homeostasis. review explores players neuroinflammation, focus on role microglia, pathways underlying intercellular communication, potential approaches mitigate neuroinflammatory damage diseases.

Язык: Английский

Процитировано

0