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Convalescent Plasma and Antibody Therapy in COVID-19
Published in Debmalya Barh, Kenneth Lundstrom, COVID-19, 2022
Didem Rıfkı, Eymen Ü. Kılıç, Şükrü Tüzmen
IFNs (IFN-I, IFN-α/β) provide a form of natural antiviral protection during the early stages of viral infection. In the later stages of the disease, the number of proinflammatory interleukins (IL-1 β, IL-6), TNF-α, and C-C motif chemokine ligands (CCL-2, CCL-3, and CCL-5) increase while IFNs decrease. Along with the decreased secretion of IFN, antiviral responses are also hampered by the reduced IFN secretion, which in return is accompanied by a rise in chemokine release attracting a large number of inflammatory cells, such as monocytes and neutrophils. This will result in an excessive inflammatory response. Mononuclear macrophages are activated by the delayed release of IFN-α/β via receptors on their surfaces. CCL2, CCL7, and CCL12, which are monocyte chemoattractants, are released by activated mononuclear macrophages, causing an increase in the number of mononuclear macrophages, which leads to increased levels of proinflammatory cytokines (IL1-, IL-6, and TNF-α) [5].
Innate Immune System in Cardiovascular Diseases
Published in Shyam S. Bansal, Immune Cells, Inflammation, and Cardiovascular Diseases, 2022
Benjamin J. Kopecky, Kory J. Lavine
Stimulation of the sympathetic nervous system triggers the release of adrenaline and noradrenaline, which results in the maturation and emigration of myeloid cells, favors the production of CCR2+ precursors [34, 113, 117], and mobilizes monocytes to the spleen [118]. Classical monocytes are rapidly recruited to the infarct (~50% from a splenic reservoir) via MCP-1 [17, 119, 120]. Splenectomy post-myocardial infarction is protective and limits myocardial inflammation [121]. During this time, there are high levels of inflammatory cytokines such as TNF-α, IL-1β, and IL-6 [122] and proteases [123]. Blockade of monocyte recruitment improves outcomes in murine models of myocardial infarction [124, 125]. CCL2 and CCL7 deficiency inhibits monocyte recruitment post-myocardial infarction and attenuates adverse remodeling [119]. Loss of Nr4a1 (responsible for converting classical to non-classical monocytes) increases classical monocyte and pro-inflammatory macrophage abundance and results in worsening heart function [122]. It is believed that CCR2+ macrophages, monocytes, and neutrophils impact collateral damage to the myocardium and accelerate adverse remodeling [110]. While there is a rapid influx of leukocytes, their persistence within the infarct is short lived (average is 20 hours). Most rapidly infiltrating innate immune cells undergo cell death, with a smaller number of cells exiting the heart and accumulating in the liver, lymph nodes, or spleen [116].
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
CCL3, also known as macrophage inflammatory protein (MIP)-1α, was shown to be upregulated in NP cells isolated from rat and human IVD tissue following treatment with IL-1β or TNF-α. In the same study, CCL3 expression in human samples was shown to be correlated with the grade of tissue degeneration (Wang et al. 2013). This molecule induced macrophage migration after treatment with NP cells conditioned media (previously treated with IL-1β or TNF-α); migration was suggested to occur via CCR1, the primary receptor of CCL3, since its inhibition resulted in cell migration blockage (Wang et al. 2013). CCL2 and CCL3 gene expression were shown to be significantly up-regulated in both human AF and NP cells after treatment with IL-1β (Liu et al. 2017b; Wang et al. 2013). Additionally, some of those chemokines, such as CCL2, CCL7, and CXCL18, have been correlated with histological degenerative tissue changes (Phillips et al. 2013) and are known to be involved in the recruitment of immune cells to inflammatory sites (Luster 1998).
Obesity, Inflammation, and Advanced Prostate Cancer
Published in Nutrition and Cancer, 2021
Armando Olivas, Ramona Salcedo Price
Adipokines, particularly the C-C chemokine receptor type 3 (CCR3)/C-C motif chemokine ligand 7 (CCL7) signaling axis, have been implicated in the link between obesity and increased metastatic capacity of PCa tumors. Recent In Vivo and In Vitro research demonstrates the adipokine CCL7, also referred to as monocyte-chemotactic protein (MCP)-3, can passively diffuse into the prostate peripheral zone and establishing a chemotactic gradient capable of attracting PCa tumor cells expressing the CCL7 receptor, CCR3 (39). The chemotactic gradient established by the invading adipokine facilitates tumor cell escape from prostate confinement and may be particularly amplified in a state of obesity as hypertrophic adipocytes are capable of secreting larger amounts of adipokines (39). It should be noted the CCR3/CCL7 signaling axis has also been implicated in metastasis in other cancer types as well and CCR3 expression correlates with Gleason score, biochemical recurrence, and surgical treatment failure of PCa (39,40). Furthermore, the proximity of PPAT to the prostate may potentiate the chemotactic effect of CCL7. As previously discussed, the obesity-associated pro-inflammatory cytokines IL-6, IL-1β, and TNFα, all to be discussed below, are also capable of mediating disease progression.
Promoting plaque stability by gene silencing of monocyte chemotactic protein-3 or overexpression of tissue factor pathway inhibitor in ApoE-/- mice
Published in Journal of Drug Targeting, 2021
Yong Zhao, Wenjia Chen, Yue Liu, Hui Li, Jinyu Chi, Qing Chang, Li Shen, Runan Yan, Jiashu Li, Xinhua Yin, Yu Fu
AS is a chronic inflammatory disease [3,4] and studies have confirmed that inflammatory reactions throughout the entire progression of AS are closely related to plaque vulnerability. Chemokines, which can lead to the formation of atherosclerotic plaques and plaque instability, play a vital role in the inflammation-mediated process of AS [5,6]. The chemokine MCP-3, also named as chemokine (C-C motif) ligand 7 (CCL7), is considered as a MCP subfamily of CC chemokines, which comprises MCP-1/CCL2 [7]. Studies have indicated MCP-1 expressed in atherosclerotic lesions plays a dominant role in the formation of atherosclerotic plaques [8]; however, comparatively little is known about the function of MCP-3 in atherosclerotic plaques. MCP-3 can regulate monocyte/macrophage accumulation and activation, and recruit monocytes from the blood into the vascular endothelium of lesion sites; these events are key in the inflammatory response in AS [7]. A study by An et al. [9] revealed that MCP-3-overexpressing transgenic mice showed an increase in lipid accumulation in the aorta; however, the relationship between MCP-3 and the plaque stability is still not clear.
PTEN negatively regulates the expression of pro-inflammatory cytokines and chemokines of fibroblast-like synoviocytes in adjuvant-induced arthritis
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Xiao-Feng Li, Xin Chen, Jing Bao, Le Xu, Lei Zhang, Cheng Huang, Xiao-Ming Meng, Jun Li
Along with FLSs activation and migration that is stimulated by several chemokines including CCL2 and CCL3 and these chemokines are abundantly expressed in the RA synovium, these chemokines may facilitate fibroblast recruitment to the synovium and subsequently induce activation of FLSs [32]. Interestingly, we also have measured inhibition of PTEN expression with bpv or PTEN-RNAi that could active the expression of CCL2 and CCL3 in AIA FLSs. Chemokines regulate chemotaxis in nearby responsive cells and are implicated in chronic inflammatory diseases, such as RA, atherosclerosis and adipose inflammation [33]. Furthermore, overexpression of PTEN with PTEN-GV141 could down-regulate expression of CCL2 and CCL3 mRNA in AIA FLSs. Rump et al. [34] proved the chemokines CCL7, CCL14, CCL16 and CCL22 occurred in RA synovial fluid and endothelial cells and have a highly significant correlation with the level of anti-CCP. In addition, with bpv or PTEN-RNAi of FLSs, the mRNA expression of VCAM-1 and VEGF-α were improved evidently. It has been proved that the serum VCAM-1 levels increased in RA, which could possibly be associated with the autoimmune and inflammatory reactions found in RA [35]. The VEGF-α is the most potent proangiogenic factor in RA angiogenesis and promotes the formation of invasive pannus, a thickened layer of synovial tissue that erodes cartilage and bone. More importantly, over-expression of PTEN with PTEN-GV141 reduced expression of VCAM-1 and VEGF-α mRNA. Consequently, PTEN also negatively regulates the expression of chemokines, VCAM-1 and VEGF-α of FLSs in AIA rats.