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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].
Microglial Voltage-Gated Proton Channel Hv1 in Neurological Disorders
Published in Tian-Le Xu, Long-Jun Wu, Nonclassical Ion Channels in the Nervous System, 2021
Madhuvika Murugan, Long-Jun Wu
Upon activation, microglia express a unique signature of cell surface and intracellular markers, and secrete different factors, depending on the state of activation. Although previously classified more rigidly as either M1 or M2 phenotype, recently it is believed that microglia exist in a spectrum of state ranging from M1 to M2 phenotypes (Ransohoff and Perry 2009, Ransohoff 2016, Qin et al. 2019). The use of Hv1 KO mice indicated that microglial Hv1 is capable of regulating microglial polarization. In fact, lack of Hv1 shifted the milieu from a predominantly pro-inflammatory M1 state to an anti-inflammatory M2 state, with increased expression of M2 markers (Arg1 and CD206) and relative reduction of M1 markers (iNOS and CD16/32) (Tian et al. 2016). In line with this, an unbiased cytokine array showed that injury-induced increase in expression of CXCL13, C5/C5a, CXCL10, M-CSF, CCL2, CCL12, CXCL12, TIMP-1, TNFα, and TREM-1 in the spinal cord was prevented in Hv1 KO mice, suggesting Hv1 is capable of modulating cytokine expression (Murugan et al. 2020). However, further studies are needed to confirm if there is a direct association between Hv1 activation, cytokine production, and microglial polarization, and investigate the underlying mechanisms.
Infection-driven periodontal disease
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Thomas E. Van Dyke, Mike Curtis
PAMP-mediated amplification of inflammation impacts leukocytes, fibroblasts, mast cells, endothelial cells, dendritic cells, and lymphocytes. Release of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, and IL-12), chemoattractants (CXCL8, CCL3, CXCL2, CCL2, and CCL12), and prostaglandin E2 (PGE2) by neutrophils, macrophages, fibroblasts, and mast cells in the connective tissue promotes collagen degradation. Mast-cell degranulation results in the secretion of histamine and leukotrienes.
Persistent changes in expression of genes involved in inflammation and fibrosis in the lungs of rats exposed to airborne lunar dust
Published in Inhalation Toxicology, 2023
Ye Zhang, Michael Story, Samrawit Yeshitla, Xiaoyu Wang, Robert R. Scully, Corey Theriot, Honglu Wu, Valerie E. Ryder, Chiu-wing Lam
Expression of the chemokine genes Ccl3, Ccl12, and Cxcl2 was closely correlated with total cell number in the BALF, and even more closely correlated with neutrophil number, especially in the samples collected 13 wk after the LD exposure. The correlation test results were presented in the Supplemental Data Table 7. As an example, the correlation of Ccl3 expression levels to neutrophil numbers (within the control, 20.8 and 60.6 mg/m3 groups) was 0.89 (p < 0.00001) and for macrophages it was 0.36 (p = 0.186) 13 wk after exposure to LD. The overall correlations of Ccl3 expression to neutrophil and macrophage numbers are presented in Figure 6(B). These results suggest that this chemokine might have played a role in recruitment of these cells into the lung in response to LD exposure. In addition, the expression of Cxcl2 was consistent with the dose- and time-dependent increases in oxidative contents of the lavage BAL cells from LD-exposed rats, as assessed by the magnitude of chemiluminescent signal production (Figure 6(C)).
Clinically feasible and prospective immunotherapeutic interventions in multidirectional comprehensive treatment of cancer
Published in Expert Opinion on Biological Therapy, 2021
Victor I. Seledtsov, Alexei von Delwig
Cellular TME components mentioned above establish a local immunosuppressive milieu not only by way of secreting certain cytokines and growth factors, such as transforming growth factor-beta (TGF-β), vascular endothelial growth factor (VEGF), and interleukin 10 (IL-10), but also by recruiting immunosuppressive cells, including regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs) [8]. In addition, tumor cells themselves can often secrete chemokines, such as C-C motif ligand 2 (CCL2) or CCL12, which down-regulate effector T cell functions [9,10]. A variety of tumors are also characterized by elevated expression of immunosuppressive tryptophan converting enzyme (IDO-1), which under physiological conditions metabolizes tryptophan and limits T- and NK-cell activation in local tissue microenvironments, such as the placenta. IDO-1 has been also shown to inhibit T-cell proliferation either by depleting local tryptophan stores or by inducing IDO-1 metabolite-mediated apoptosis [10,11]. Tumor progression is also dependent on extracellular adenosine triphosphate (ATP)/adenosine (ADO) interrelationship, with ATP stimulating anti-tumor immune responses and ADO (main metabolite of ATP) down-regulating anti-tumor immunity. The latter fact can be at least partially explained by an observation that increased ADO levels are associated with dysfunctional T cell, NK cell, and B cell compartments [12].
Large animal models for translational research in acute kidney injury
Published in Renal Failure, 2020
Balamurugan Packialakshmi, Ian J. Stewart, David M. Burmeister, Kevin K. Chung, Xiaoming Zhou
Neutrophils are the most abundant type of granulocytes and make up 40–70% of all white blood cells in humans. They are also the most abundant leukocytes infiltrating the kidney immediately after IRI [37]. Neutrophils produce and secrete cytotoxic compounds such as reactive oxygen species, while adhering to the endothelium and extravagating into the affected renal tissue. CXCL8/IL-8 is the primary chemoattractant for human neutrophil recruitment. Serum CXCL8/IL-8 levels predict AKI in patients with acute pancreatitis [38], after cardiac surgery [39] and liver transplantation [40]. Conversely, CCL12 probably mediates tubular regeneration and functional recovery from cisplatin-induced AKI following inhibition of dipeptidyl peptidase-4 in a murine model [41]. Given the important roles that these molecular pathways play in the development of AKI, it becomes apparent that immunomodulatory findings from rodent AKI models may have certain limitations [19].