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The Opioid Epidemic
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
Chemokine and cytokine secretion from microglia and lymphocytes contributes to analgesic tolerance. After chronic morphine exposure, the chemokine fractalkine (CX3CL1) can be cleaved from the neuron cell membrane changing from the inactive form into the active form. This cleavage occurs secondary to glutamate signaling, presumably from opioid-induced NMDA receptor activation. CX3CL1 can bind to its CX3CR1 receptor on microglia. CX3CL1 induces the release of IL-1 from the spinal cord which opposes morphine analgesia. Co-administration of morphine with a neutralizing antibody against CX3CL1 potentiated acute morphine analgesia and attenuated the development of tolerance, hyperalgesia, and allodynia.26 The same occurs in the periaqueductal grey (PAG).27
The Promise for Alzheimer’s Disease Treatment
Published in Dilip Ghosh, Pulok K. Mukherjee, Natural Medicines, 2019
Víctor Andrade, Leonardo Guzmán-Martínez, Nicole Cortés, Ricardo B. Maccioni
Recent reports have demonstrated that after the microglial cells are activated, they overexpress several receptors and ligands belonging to the main chemokine families (CC, CXC and CX3C). Some of these are also expressed in astrocytes, which suggests that chemokines may serve as communication signals between them and microglia. It has been proposed that CX3CR1 and its ligand, fraktalkine (CX3CL1), which are expressed in neurons, also play a paramount role in neuronal signalling with the microglial cells (Rock et al. 2004). There are diverse factors regulating the phagocytic activity of microglial cells, one of which is the chloride intracellular channel (CLIC1). Pharmacological inhibition of this channel or negative regulation of its expression at the transcriptional level by an interference RNA alters the normal phagocytic activity of the microglia. On the other hand, it has been reported that the ciliary neurotrophic factor (CNTF) promotes phagocytosis in a way mediated by Ca2+ (Lee et al. 2009). In conclusion, microglial cells can receive stimulus from environmental agents or endogenous proteins, which triggers an over-activated state, releasing pro-inflammatory factors, ROS, reactive nitrogen species (RNS) and evoking toxicity in the vicinity of neuronal population (Innamorato et al. 2009).
Cell Recruitment for Intervertebral Disc
Published in Raquel M. Gonçalves, Mário Adolfo Barbosa, Gene and Cell Delivery for Intervertebral Disc Degeneration, 2018
Catarina Leite Pereira, Sibylle Grad, Mário Adolfo Barbosa, Raquel M. Gonçalves
Similar to what has been described in the mobilization process of stem cells, chemokines and their receptors play an important role in immune cell mobilization and localized response (Surmi and Hasty 2010). These factors do not only guide the cells to target sites of infection and inflammation, but also they coordinate the interaction between these cells, thereby providing the appropriate and optimal adaptive immune response against pathogens, tumor cells, or dead cells (Sokol and Luster 2015). For example, in immune cell development, SDF-1α/CXCR4 interactions remain essential for BM retention and normal development of several immune cells, such as B cells, monocytes, macrophages, neutrophils, natural killer cells, and plasmocytoid dendritic cells (DCs) (Mercier, Ragu, and Scadden 2011). Monocyte exit from the BM seems to be dependent on CXCR4 and CCR2 in homeostatic conditions. Monocytes may further differentiate into proinflammatory (CCR2+) or anti-inflammatory (CX3CR1+) subsets. CX3CR1 expressing monocytes are thought to migrate to the periphery under CX3CL1 gradients and might develop into tissue macrophages following additional chemokine signals (Sokol and Luster 2015). Eosinophils released from the BM to the peripheral tissues are largely dependent on CCL11/CCR3 interactions, while basophil release is mainly mediated by CXCR4, although they constitutively express CXCR1, CCR1, CCR2, and CCR3 (Iikura et al. 2001; Palframan et al. 1998).
Urinary IgG, serum CX3CL1 and miRNA-152-3p: as predictors of nephropathy in Egyptian type 2 diabetic patients
Published in Tissue Barriers, 2022
Aml E Abdou, Haneya A.A. Anani, Hanan F. Ibrahim, Eman Elshohat Ebrahem, Nora Seliem, Eman M.I. Youssef, Niveen M. Ghoraba, Asmaa S. Hassan, Marwa A. A. Ramadan, Eman Mahmoud, Shorouk Issa, Hend M. Maghraby, Eman K. Abdelrahman, Hala Ali Mohammed Hassan
C-X3-C motif chemokine 2 (CX3CL1) upregulated in diabetes produced mostly by glomerular endothelial cells and the tubular epithelium and as well as in many other cells, such as podocytes, stromal cells and renal tumor cells.8 CX3CL1, also known as fractalkine. CX3CL1 has two types (membrane and soluble). Membrane CX3CL1 is an adhesion molecule, but it is a chemoattractant for Chemokine (C-X3-C motif) Receptor 1 (CX3CR1+ cells) in the soluble form.9 The most of leukocytes that invade the kidney during nephropathies were shown to express CX3CR1. Chemokine (C-X3-C motif) receptor 1 (CX3CR1) is frequently expressed on monocytes and T cells in most organs. CX3CL1 is the only ligand for CX3CR1, a single chemokine acts as a chemoattractant as well as helps CX3CR1+ cells bind together. As a result, the CX3CL1/CX3CR1 axis represents a novel type of leukocyte-migration regulator.10 Furthermore, it has a role in the enhancement of chronic renal disorders like DN.11 High glucose levels, AGE formation, and cytokine activation in diabetes may induce fractalkine upregulation in the kidneys and lead to progression of diabetic nephropathy12 (McDermott et al. 2003).
Diminished levels of the chemokine fractalkine in post-mortem prefrontal cortex in schizophrenia but not bipolar disorder
Published in The World Journal of Biological Psychiatry, 2021
Sarah L. Hill, Li Shao, Clare L. Beasley
In addition to a recognised role in the immune system, the fractalkine pathway has more recently been implicated in the regulation of synaptic function. In particular, CX3CR1 knock-out mice display a transient deficit in synaptic pruning during brain development, potentially via impaired microglial function (Paolicelli et al. 2011). In our study CX3CR1 protein levels were highly correlated with levels of the presynaptic protein SNAP-25 in the control group, with the strength of this correlation significantly reduced in SCZ. While the mechanisms underlying this relationship remain unclear, given evidence for reduced presynaptic density in SCZ (Honer and Young 2004), further investigation into the contribution of microglial cells to synaptic dysregulation in this disorder is warranted.
Cytotoxic Tph-like cells are involved in persistent tissue damage in IgG4-related disease
Published in Modern Rheumatology, 2021
Hayato Yabe, Ryuta Kamekura, Motohisa Yamamoto, Kosuke Murayama, Shiori Kamiya, Ippei Ikegami, Katsunori Shigehara, Hiromi Takaki, Hirofumi Chiba, Hiroki Takahashi, Kenichi Takano, Hiroki Takahashi, Shingo Ichimiya
We have recently reported granzyme A+ Tph-like cells and their potential role in the pathogenesis of IgG4-RD [8]. Following our observations in that study, we performed this study to analyze Tph-like cells by means of t-SNE and identified features of Tph-like cells in IgG4-RD, which highly expressed granzyme A and CX3CR1 (Figure 3(A)). It is well known that fractalkine and CX3CR1 are related to chronic inflammation in several diseases such as autoimmune vasculitis and Sjögren syndrome [18,29]. Therefore, we focused on the fractalkine-CX3CR1 axis and found cytotoxic CX3CR1+ Tph-like cells comprising one of the CD4+ CTL subsets. It is possible that CX3CR1+ Tph-like cells play an important role in the pathogenesis of other chronic inflammatory diseases. Due to the limitation in obtaining blood samples from patients with other chronic inflammatory diseases such as Sjögren syndrome, we could not analyze a sufficient number of unfrozen blood samples for this study. Their roles in the pathogenesis of other chronic inflammatory diseases need to be explored in future studies.