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AI and Autoimmunity
Published in Louis J. Catania, AI for Immunology, 2021
As the immune system fights off foreign antigens, it is continually releasing inflammatory proteins called “pro-inflammatory cytokines.” If the pathological antigen is not successfully eliminated in a timely fashion, the pro-inflammatory cytokines accumulate in the tissue in abnormal amounts and are interpreted by the adaptive immune system as antigenic (foreign) and perpetuate an autoimmune response.
Mechanisms of Nanotoxicity to Cells, Animals, and Humans
Published in Vineet Kumar, Nandita Dasgupta, Shivendu Ranjan, Nanotoxicology, 2018
Belinda Wong Shu Ee, Puja Khanna, Ng Cheng Teng, Baeg Gyeong Hun
Numerous studies have shown that nanoparticle-mediated ROS generation can cause inflammation. Exposure to SWCNTs induced ROS production, resulting in the transcriptional activation of pro-inflammatory transcription factors such as nuclear factor-κB (NF-κB), activator protein 1 (AP-1), and Akt in human mesothelial cells (Pacurari et al. 2008). Similarly, MWCNT induced oxidative stress which subsequently activated NF-κB signaling cascade and promoted inflammatory cytokines secretion in the macrophage RAW264.7 cells. Inflammatory cytokines secreted by the cells included tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and interleukin-10 (IL-10) (He et al. 2011). In vivo studies using ICR mice injected with SiNPs also showed elevated levels of IL-1β and TNF-α in cultured peritoneal macrophages harvested from the treated mice (Park and Park 2009). In summary, nanoparticle-mediated ROS production is determined by their physicochemical properties, such as sizes and surface properties, as well as the type of nanoparticles. Upon gaining cellular entry, nanoparticles cause mitochondria damage and/or depletion of antioxidant species, both of which lead to a build-up of oxidative stress (Figure 11.2). Subsequently, the excess ROS generated in cells lead to DNA damage, lipid peroxidation, protein oxidation, and inflammation (Figure 11.3).
Applications of Biotechnology: Biology Doing Chemistry
Published in Richard J. Sundberg, The Chemical Century, 2017
Tumor necrosis factor (TNF) is one of the primary cytokines that initiates and controls the inflammatory process (see Section 13.1.1). As such, it is of interest in treatment of arthritis and other autoimmune conditions. Particular attention has been given to treatment of arthritis, including juvenile arthritis which affects children and adolescents. Several types of agents have been developed by biotechnology and applied to the treatment of arthritis. The main side effect of the TNF inhibitors is to suppress immunity to infectious diseases, including relative common infections such as sinusitis, but also tuberculosis. An important current issue with these drugs is whether they must be continued or if remission can be maintained after reduction or elimination of the drugs. The three bestselling biologic drugs are in this group are Enbrel, Humira, and Remicade, all of which had sales exceeding $6 billion in 2010. Etanercept (brand name Enbrel) is a fusion protein of AA 1–235 of TNF and AA 236–467 of human immunoglobulin. It shows significant improvement in treatment of juvenile arthritis and can be used in combination with other drugs used to treat that condition, including methotrexate. It functions by binding to TNF-α, thus blocking its pro-inflammatory effects. While original recommendations were for use if standard therapies failed (e.g., methotrexate or anti-inflammatory steroids), there are now recommendation that aggressive therapy be started early. Adalimunmab (Humira) is a monoclonal antibody to human TNF. There are several other monoclonal antibodies that are used in treatment arthritis and other auto-immune conditions. In addition to the original approval for arthritis (2002) and juvenile arthritis (2008), adalimumab has also been approved for several other auto-immune diseases. Other examples include infliximab (Remicade), certolizumab (Cimzia), and golimumab (Simponi). These materials act by inhibiting the pro-inflammatory effects of TNF. Other drugs are targeted at other pro-inflammatory cytokines, for example, tocilizumab (Actemra),22 which is targeted at interleukin-6 (IL-6). Tocilizumab binds to the IL-6 receptor, blocking the effect of the inflammatory effect of the cytokine.
Co(II)-coordination polymer: treatment and nursing values on trachoma by inhibiting the Chlamydia trachomatis survival
Published in Inorganic and Nano-Metal Chemistry, 2022
Yan Yang, Lei Shao, Dong-Li Zhao
The ELISA detection assay was performed and the levels of the inflammatory cytokines was measured. This preformation was finished under the guidance of the instructions with some modifications. In brief, the conjunctival fibroblast in the logical growth phage were collected and seeded into the 96 well plates at the concentration of 104 cells per well. The cells were placed in an incubatory at the condition of 37 °C, 5%CO2 for 12 h. Then, the Ct was added to infect the conjunctival fibroblast at the MOI of 30:1, which was followed by the compound treatment at 1, 2 and 5 mg/mL. The compound power was firstly solved in the DMSO solution, and then diluted into the indicated concentration with PBS solution. Next, the cell supernatant was harvested, centrifuged to remove the Ct, and the levels of the inflammatory cytokines released by conjunctival fibroblast was measured with ELISA detection kit.
Significance of LED lights in enhancing the production of vinegar using Acetobacter pasteurianus AP01
Published in Preparative Biochemistry & Biotechnology, 2022
Jeong-Muk Lim, Seong-Hyeon Lee, Do-Youn Jeong, Seung-Wha Jo, Seralathan Kamala-Kannan, Byung-Taek Oh
During an inflammatory response, various pro-inflammatory cytokines work as initiators and mediators. TNF-α and IL-6 are the major cytokines produced by activated RAW 264.7 cells, and their excessive production leads to inflammatory diseases.[53] Therefore, the inhibitory activity of vinegar on TNF-α and IL-6 production can be important for inflammatory disease prevention and treatment. As shown in Figure 7, production of TNF-α and IL-6 was greatly increased due to stimulation of LPS. The co-treatment of LPS and vinegar did not significantly reduce the production of TNF-α, but the production of IL-6 was significantly reduced in a concentration-dependent manner for vinegar. Especially, it was confirmed that the treatment with vinegar (4%) fermented under red and green LEDs greatly inhibited the production of IL-6 by 61% and 59%, respectively. The results confirmed that vinegar fermented under LED conditions inhibit the production of IL-6 in LPS-stimulated RAW 264.7 cells, which may play an important role in the anti-inflammatory process.
Heterometallic La(III)-Co(II) coordination polymers: treatment activity on diabetic foot by reducing the TLR-4–NF-κB signaling pathway activation in the plantar tissue
Published in Inorganic and Nano-Metal Chemistry, 2020
Rui Shao, Dai Li, Ming-Yi Zhang, Jing Zhao, Xiao-Mei Tan, Yong-Qiang Zhang
In the above research, we have successfully synthesized compounds 1 and 2 with novel structure. Then, in this present experiment, the enhancement activity of these two compounds on the therapeutic effect of improved negative pressure suction for DF was assessed, and the related mechanism was explored at the same time. As reported, there was usually combined with a significantly increased level of the inflammatory response in the plantar tissue. So, the inflammatory cytokines content was measured with the ELISA detection kit. As the results shown in Figure 4, we can see that different from the control group, the content of the IL-1β and TNF-α in the model group was obviously increased. However, this abnormal increase of the inflammatory cytokines could be reduced by compound 1 treatment, while compound 2 showed only a slightly inhibitory effect on the level of the inflammatory cytokines in the plantar tissue.