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Epidemiology and Pathogenesis of COVID-19
Published in Hanadi Talal Ahmedah, Muhammad Riaz, Sagheer Ahmed, Marius Alexandru Moga, The Covid-19 Pandemic, 2023
Sidrah Tariq Khan, Sagheer Ahmed
Other cells released in the event of a viral infection include inflammatory cytokines; TNF-α, IL-6, 2, and 10, IFN-α/-γ, Granulocyte-macrophage colony-stimulating factor (GM-CSF), monocyte chemotactic protein 3 (MCP3), macrophage inflammatory protein 1-α (MIP 1 α), which have shown enhanced levels after infection with a coronavirus leading to the migration of inflammatory cells in the lungs resulting in ARDS which has a high mortality rate especially in critical patients. Along with cytokines, increased levels of chemokines such as CCL2/MCP1, interferon gamma-induced protein 10 (IP-10), CXCL1 as well as CXCL5 have also been observed. One study carried out a transcriptomic analysis on infected peripheral blood mononuclear cells (PBMCs) and infected cells from the patient’s bronchoal-veolar lavage fluid (BALF) to ascertain host responses. The results showed an upregulation of inflammatory cytokines such as CCL2, CXCL2, CCL8, CXCL1, IL33, CCL3L1 in the BALF and CXCL10, TNFSF10, TIMP1, C5, IL18, AREG, NRG1, IL10 in the PBMCs which led to a cytokine storm in patients causing severe inflammation in the lungs. Moreover, further analysis also revealed activated apoptotic and P53 signaling pathways that could be the reason behind the lymphopenia seen in many severely ill COVID-19 patients [12].
Cholecystectomy-induced secondary bile acids accumulation ameliorates colitis through inhibiting monocyte/macrophage recruitment
Published in Gut Microbes, 2022
Yun Liu, Jun Xu, Xinhua Ren, Yu Zhang, Ziliang Ke, Jianhua Zhou, Yang Wang, Yifan Zhang, Yulan Liu
Based on the results mentioned above, secondary BAs inhibited inflammatory cytokines and monocytes chemoattractant proteins. We tried to identify the mechanism by which secondary BAs were at work in vitro. After differentiation into macrophages, THP-1 derived macrophages were cultured with 20, 50, 100, and 200 μM specific secondary BAs (LCA, DCA, or HDCA) for 24 h and then stimulated with LPS for one hour (Figure 7a). Data showed that the LCA, DCA, or HDCA inhibited mRNA levels of LPS-induced chemokines (CCL2, CCL8, Figure 7b,c) and inflammatory cytokines (IL6, IL1β, Figure 7d,e) responses in a dose-dependent manner. We also tested several BARs levels in THP-1 derived macrophages. As a result, there were dose-dependent increased effects of LCA, DCA, or HDCA on Nr1h3 (LXRα) levels (Figure 7f), rather than other BARs (Figure S6a-d). Furthermore, the cells were pretreated with 100 μM secondary BAs and an LXR inhibitor GSK2033, then stimulated with LPS for one hour (Figure 8a). The inhibiting effects of DCA or HDCA on chemokines (CCL2, CCL8) were abrogated in the presence of LXR inhibitor (Figure 8b,c), but inflammatory cytokines (IL6, IL1β) were still suppressed (Figure 8d,e). The LXRα signaling seemed noncontributory in LCA-restrained chemokines secretions in macrophages (Figure 8b-e).
Association between the Genetic Polymorphisms of CCL2, CCL5, CCL8, CCR2, and CCR5 with Chronic Hepatitis C Virus Infection in the Chinese Han Population
Published in Immunological Investigations, 2022
Lin-Nan Shao, Shi-Hang Zhou, Ni Wang, Shu-Ting Zhang, Ming Liu
We measured the plasma levels of CCL2, CCL5, CCL8, CCR2, and CCR5 in healthy controls. No significant differences were identified between the SNPs/haplotypes and plasma levels of CCL2, CCL5, CCL8, CCR2, and CCR5 suggesting that these SNPs/haplotypes do not influence the plasma levels of CCL2, CCL5, CCL8, CCR2, and CCR5 in healthy individuals. However, contradictory findings have been reported from other studies regarding the influence of rs1024611 on the serum/plasma levels of CCL2 in healthy controls (Alegret et al. 2013; He et al. 2017; Joven et al. 2006; Wei et al. 2015). We speculated that this discrepancy may be owing to the following: (1) variations in the frequencies of alleles and haplotypes in different ethnic populations, which provide a potential reason that results may not always be replicated in other populations; (2) limited sample size and different inclusion/exclusion criteria of the enrolled subjects; and (3) other factors that also contribute to the plasma levels of these components.
Prospects of cell chemotactic factors in bone and cartilage tissue engineering
Published in Expert Opinion on Biological Therapy, 2022
Ke Chen, Hui Gao, Yongchang Yao
In addition, Chemokines include a variety of cytokines, inflammatory regulators and cell migration regulators that play a significant role in processes such as angiogenesis, cardiogenesis, trauma repair and regeneration [49,124]. During the wound healing process, chemokines coordinate the healing process through the recruitment of inflammatory cells and the regulation of angiogenesis, and inflammatory cells secrete growth factors and cytokines to promote wound healing [125]. In the presence of chemokines, stem cells secrete angiogenic factors such as vascular endothelial growth factor, transforming growth factor-beta, matrix metalloproteinase and other chemokines to promote angiogenesis [38,126]. The secretion of immunomodulatory and inflammatory chemokines, including transforming growth factor-beta, tumor necrosis factor-alpha (TNF-alpha), CCL2, CCL3 and CCL8, prevents the proliferation of effector T cells, promotes a regulatory phenotype of leukocytes and regulates the immune response in vivo [127–129].