China
Africa
Explore chapters and articles related to this topic
Innate Immune System in Cardiovascular Diseases
Published in Shyam S. Bansal, Immune Cells, Inflammation, and Cardiovascular Diseases, 2022
Benjamin J. Kopecky, Kory J. Lavine
In the subacute phase, the combined innate and adaptive immune system effectively eliminates infected and dead cells but also contributes to myocardial damage. Removal of macrophages early in viral myocarditis resulted in early mortality, while removal in the chronic phase led to improved cardiac function and decreased adverse remodeling [132]. Deletion of CX3CL1 or its receptor (CX3CR1) worsens acute viral myocarditis [133]. Interference with monocyte recruitment by inhibiting CCL2 or CCL3 signaling reduced cardiac injury [134]. These data suggest that macrophages and monocytes may have distinct and temporally restricted functions in viral myocarditis. Consistent with this, tissue-resident macrophages secrete anti-inflammatory TGF-β and IL-10, promoting the resolution of inflammation and wound healing [135], an event essential to preventing autoimmune responses that perpetuate cardiac dysfunction. In experimental models of autoinflammatory myocarditis, the activation of monocytes and macrophages appears to promote chronic heart failure. Targeting of monocytes through blockade of the CCR2/CCL2 axis improves outcomes through a reduction of monocyte infiltration and differentiation into dendritic cells and monocyte-derived macrophages [131, 136].
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).
Expression of interferon-stimulated gene 20 (ISG20), an antiviral effector protein, in glomerular endothelial cells: possible involvement of ISG20 in lupus nephritis
Published in Renal Failure, 2023
Takao Karasawa, Riko Sato, Tadaatsu Imaizumi, Masashi Fujita, Tomomi Aizawa, Koji Tsugawa, Deborah Mattinzoli, Shogo Kawaguchi, Kazuhiko Seya, Kiminori Terui, Kensuke Joh, Hiroshi Tanaka
Polyinosinic-polycytidylic acid (poly IC), lipopolysaccharide (LPS) from Escherichia coli, and an actin antibody were obtained from Sigma-Aldrich (St Louis, MO, USA). The TLR7 ligand R848 and TLR9 ligand CpG were purchased from InVivoGen (San Diego, CA, USA) and Novus Biologicals (Centennial, CO, USA), respectively. The Illustra RNAspin kit was obtained from GE Healthcare (Buckinghamshire, UK). The rabbit antibodies against ISG20 and IFIT1 were purchased from GeneTex (Irvine, CA, USA). Lipofectamine RNAiMAX reagent, Moloney murine leukemia virus (MMLV) reverse transcriptase, dNTP mix, and small interfering RNA (siRNA) against IFN-β were obtained from Thermo Fisher Scientific (Waltham, MA, USA). The siRNAs against ISG20 and a non-targeting negative control siRNA were obtained from Qiagen (Hilden, Germany). The SsoAdvanced Universal SYBR Green Supermix was obtained from Bio-Rad (Hercules, CA, USA). Horseradish peroxidase (HRP)-conjugated anti-rabbit antibodies were obtained from Medical and Biological Laboratories (Nagoya, Japan). Polyvinylidene difluoride (PVDF) membranes and Luminata Crescendo Western HRP substrates were obtained from Merck Millipore (Darmstadt, Germany). The enzyme-linked immunosorbent assay (ELISA) kit for CX3CL1 was obtained from R&D Systems (Minneapolis, MN, USA).
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).
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
In this study, we focused on CX3CR1 in Tph-like and tried to clarify its role in the pathogenesis of IgG4-RD. The chemokine fractalkine (CX3CL1) is a unique ligand that specifically binds to CX3CR1 for the coordination of inflammation as well as the wound healing process [9]. In humans, fractalkine is constitutively expressed by intestinal epithelial cells, synovial cells, macrophages, dendritic cells, neurons, and microglia [10,11]. Fractalkine is also known to be upregulated in endothelial cells upon various stimuli of inflammatory cytokines [12]. While CX3CR1 is presented by monocytes, macrophages, mucosal dendritic cells, natural killer cells, and a subset of effector memory CD4+ T cells [9,13–15], it is noteworthy that the expression of CX3CR1 is strongly linked to the cytotoxic potential of CD8+ T cells in both humans and mice [16]. This ligand-receptor pair has been proposed to contribute to inflammatory diseases such as autoimmune diseases [17,18] and allergic airway diseases [19]. In this context, fractalkine and CX3CR1 are considered as an attractive therapeutic target for immunomodulation, though their roles in the pathogenesis of IgG4-RD remain unknown.