hydrogen as a means of controlling and preventing COVID-19

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Yang et al. Hydrogen: Potential Therapy for COVID-19 HYDROGEN AND THE CYTOKINE STORM Immune cells can become activated, producing pro-inflammatory cytokines, including tumor necrosis factor-a (TNF-a), interleukins (such as IL-1b and IL-6), and interferon-g (IFN-g) (Taniguchi and Karin, 2018). An effect of cytokines is the activation of the NADPH oxidase in leukocytes, which leads to the production of reactive oxygen species (ROS) such as superoxide, hydroxyl radicals, and singlet oxygen (Liu et al., 2015). In 1993, Ferrara et al. first proposed the concept of a cytokine storm in graft-versus-host disease (Ferrara et al., 1993). SARS coronavirus infection was found to induce an interferon-g- related cytokine storm, which might be related to the immunopathological damage observed in SARS patients (Huang et al., 2005). In 2005, a study on avian influenza A H5N1 suggested that high viral loads and the resulting intense inflammatory response are key to its onset (de Jong et al., 2006). Cytokine storms have also been reported in influenza (Kalil and Thomas, 2019) and Middle East respiratory syndrome (MERS) (Channappanavar and Perlman, 2017). At present, the factor that causes cytokine storms is not clear, but it is generally believed that the immune system overreacts to new and highly pathogenic pathogens. The relating imbalance of the immune regulatory network, the lack of negative feedback, and the continuous self-amplification of positive feedback lead to an abnormal increase in many kinds of cytokines, and finally to a cytokine storm. Although the pathophysiological mechanism underlying COVID-19 is not completely understood, it has been reported that there are large quantities of cytokines such as IL-1 b, INF-g, IP-10, and MCP-1 in COVID-19 patients, which might activate Th1 cells. The concentrations of G-CSF, IP-10, MCP-1, MIP-IA, and TNF-a in critically ill patients were found to be higher than those in non-critical patients, indicating that cytokine storms might be related to the severity of the disease (Liu et al., 2020). The effectiveness of anti-IL6-receptor and glucocorticoid therapy for patients with COVID-19 was only verified in a small number of patients (Selvaraj et al., 2020; Xu X. et al., 2020). However, more clinical studies are underway with respect to treating COVID-19 with tocilizumab and dexamethasone (NCT04445272, NCT04244591, NCT04381364). Corticosteroids suppress lung inflammation but also inhibit immune responses and pathogen clearance (Russell et al., 2020). Furthermore, the use of anti-IL6-receptor therapy for patients with rheumatic diseases might lead to an increased risk of infection (Rutherford et al., 2018). Due to these potential side effects, tocilizumab and dexamethasone have not been widely used in clinical practice. Cytokines released excessively can cause acute lung injury in patients. An increase in TNF-a levels will lead to the activation of inflammatory cytokines such as IL-1, IL-6, and IL-8 (Chen et al., 2015). At the same time, high mobility group box1 (HMGB1) (Ma et al., 2015), CCL2 (Hillman et al., 2007), and Egr-1 (Hoetzel et al., 2008) all affect the release of inflammatory factors. Keliang Xie found that hydrogen can suppress the infiltration of neutrophils and macrophages in lung tissue, inhibit the activity of NF-kB and MPO in lung tissue, and reduce inflammatory factors and cytokine secretion in lung tissue, including TNF-a, IL-1, IL-6, and HMGB1. Hydrogen can eliminate ROS, such as hydroxyl and peroxynitrate anions, while maintaining the normal metabolism of redox reactions and other ROS (Xie et al., 2012). Accordingly, hydrogen treatment can reduce the levels of TNF-a, IL-1, IL-1 b, IL-6, IL-8, HMGB1, CCL2, and Egr-1 in lung tissue in an animal model (Huang et al., 2010a). Furthermore, inhaling hydrogen for 45 minutes can reduce airway inflammation in patients with asthma and COPD (Wang et al., 2020). At the same time, previous studies have shown that an increase in IL-10 can inhibit the synthesis and release of inflammatory cells and colony stimulating factors (Laveda et al., 2006). After inhaling hydrogen, IL-10 was found to increase in the serum and sputum supernatant of sanitation workers (Gong et al. 2016), indicating that this treatment can affect anti-inflammatory reactions and reduce secondary injury caused by cytokine storms. Some critical patients with pneumonia need to be supported by mechanical ventilation. However, this can cause lung injury or aggravate the original lung injury. In a rat model of mechanically ventilated lung injury, Huang et al. (Huang et al., 2010a) found that after inhaling 2% hydrogen the expression of NF-kappa B was activated, promoting the expression of the anti- apoptotic protein Bcl-2, inhibiting expression of the apoptotic protein Bax, suppressing inflammatory factor expression, decreasing the lung histopathological score, and alleviating pulmonary edema, thus diminishing ventilator-related acute lung injury. In addition, hydrogen can inhibit the Rho/ROCK pathway, increase the expression of ZO-1, and protect lung tissue cells by improving cell-to-cell permeability, and reducing lung injury (Zhang et al., 2016). Therefore, the early use of hydrogen in COVID-19 patients could potentially suppress the release of cytokines and reduce lung injury. HYDROGEN AND OXIDATIVE STRESS REACTIONS IN COVID-19 Superoxide dismutase (SOD) is an important antioxidant enzyme in the antioxidant defense system of the body. It can remove a variety of toxic or oxidizing substances in the body to eliminate the damage to DNA and biological functional proteins caused by these substances to maintain the stability of the internal environment and contribute to anti-toxicity and anti-oxidation processes (Gwarzo and Muhammad, 2010). After hydrogen treatment, the content of malondialdehyde in lung tissue can be reduced, increasing the activity of SOD (Shi et al. 2013). This helps to maintain the stability of the internal environment of the body to achieve excessive activation of oxidative processes and reduce the oxidative stress caused by the ROS pathway. Multiple organ failure is a common cause of death in critically ill COVID-19 patients. Hydrogen may be used to protect multiple organs including the heart, kidney, and nervous system via anti-apoptotic and anti-oxidative functions to maintain the normal response of the body and reduce mortality (Hayashida et al., 2012; Hayashida et al., 2014; Homma et al., 2014). Frontiers in Pharmacology | www.frontiersin.org 2 October 2020 | Volume 11 | Article 543718

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