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Anti-Arthritic Potential of Gold Nanoparticle
Published in Klaus D. Sattler, st Century Nanoscience – A Handbook, 2020
Jayeeta Sengupta, Sourav Ghosh, Antony Gomes
When T lymphocyte interacts with MHC on antigen-presenting cells, it may be activated, or show tolerance to the antigen, or undergo programmed cell death, depending on a second signal through appointing additional cellular receptors. The CD24 molecule on the T-cell surface may act as this second signal of costimulation. Activated T cells proliferate and secrete additional cytokines such as interleukin-2, interleukin-4, tumor necrosis factor, and interferon-γ. Interleukin-2 amplifies the proliferation of T cells. Very early inflamed synovium has been found to have an unexpected T helper cell profile, along with increased expression of interleukin-4, interleukin-5, and interleukin-13. When the diseased is established, synovial T cells produce low amounts of interferon-γ, interleukin-10, and tumor necrosis factor-α, while interleukin-2 and interleukin-4 become virtually absent. Interleukin-17 is produced spontaneously in synovial cells of rheumatoid arthritis patients. Interleukin-23 promotes the survival and proliferation of T helper cells. The receptor for interleukin-17 is expressed all over the synovium and exerts pleiotropic effects. Thus, T-cell-derived interleukin-17 (subtypes 17A and 17F) promotes monocyte-dependent interleukin-1 and tumor necrosis factor-α production and induces osteoclast differentiating factor RANKL (receptor activator of nuclear factor kappa-B ligand), stimulating synovial fibroblasts to express interleukin-6, interleukin-8, granulocyte colony-stimulating factor, prostaglandin E2, and matrix metalloproteinases.
Nanostructured Biointerfaces
Published in Šeila Selimovic, Nanopatterning and Nanoscale Devices for Biological Applications, 2017
Jean Paul Allain, Monica Echeverry-Rendón, Juan Jose Pavón, Sandra L. Arias
In the process of recognizing the presence of a biomaterial, the body activates different molecules such as mitogens, chemoattractants, cytokines, growth factors, and other bioactive molecules that can modulate the activity of macrophages, along with the proliferation and activation of other cell populations in the inflammatory and wound-healing responses, which are identified by the presence of mononuclear cells such as monocytes and lymphocytes, at the biomaterial implant site. Chemokines are cytokines that are chemoattractants. They coordinate cellular migration in inflammation to produce an efficient and effective process of wound healing and are involved in other processes such as hematopoiesis, angiogenesis, and cellular differentiation. The production of cytoquines such as interleukin-4 and interleukin-13 plays a significant role in the reaction of the body after exposure to a foreign agent [32,33].
Pathological Manifestations and Mechanisms of Metal Toxicity
Published in Debasis Bagchi, Manashi Bagchi, Metal Toxicology Handbook, 2020
Mechanisms of toxicity include activation of apoptotic pathways via Fas abd c-myc (Guo, Chen, et al., 2015) and upregulation of inflammatory response via NF-κB and impacting interleukin-2 (IL-2), interleukin-4 (IL-4), and interleukin-13 (IL-13) (Guo, Deng, et al., 2015).
Comparative electrophysiological evaluation of hippocampal function following repeated inhalation exposures to JP-8, Jet A, JP-5, and the synthetic Fischer Tropsch fuel
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Joyce G. Rohan, Shawn M. McInturf, Molly K. Miklasevich, Chester P. Gut, Michael D. Grimm, James E. Reboulet, William R. Howard, Karen L. Mumy
Approximately 100 µl blood was collected from the lateral tail vein of rats prior to initiation of exposure and within 24 hr following the last day of exposure. The following nine pro-inflammatory cytokines were determined using the Meso Scale Discovery (MSD) multiplex kit and the Sector Imager 2400 instrument: IFN-γ (interferon gamma), IL-1β (interleukin 1β), IL-4 (interleukin 4), IL-5 (interleukin 5), IL-6 (interleukin 6), IL-10 (interleukin 10), IL-13 (interleukin 13), KC/GRO (keratinocyte chemoattractant/ human growth-regulated oncogene chemokines), and TNF-α (tumor necrosis factor alpha). Cytokine levels were measured before and after the 28-d occupational exposure. Normalized data were calculated as the cytokine level (pg/ml) after last day of exposure divided by concentration before the first day of exposure. In Phase 4 (JP-5 exposure), blood was collected at baseline, following the 4th day of treatment, and within 24 hr as well as 2 weeks after completion of exposures.
Comparison of silver nanoparticle-induced inflammatory responses between healthy and metabolic syndrome mouse models
Published in Journal of Toxicology and Environmental Health, Part A, 2020
Lisa Kobos, Saeed Alqahtani, Li Xia, Vincent Coltellino, Riley Kishman, Daniel McIlrath, Carlos Perez-Torres, Jonathan Shannahan
Total RNA was isolated from each organ of the gene expression cohort and converted to cDNA. AgNP-induced variations in the inflammatory response were measured through assessment of alterations in gene expression for tumor necrosis factor-α (TNF-α), chemokine (C-C motif) ligand 2 (CCL2), chemokine (C-X-C motif) ligand 1 (CXCL1), chemokine (C-X-C motif) ligand 2 (CXCL2), interleukin 4 (IL-4), and interleukin 13 (IL-13). In addition, fibrotic marker transforming growth factor-β (TGF-β) and oxidative stress marker heme oxygenase 1 (HO-1) were assessed. Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) was used as the internal control. All genes were analyzed via real-time RT-qPCR (n = 7–8 per group).