pulmonary edema and covid vaccine

MeSH Role of Drugs Used for Chronic Disease Management on Susceptibility and Severity of COVID19: A Large CaseControl Study. doi:10.1165/ajrcmb.20.5.3382, Pascarella, G., Strumia, A., Piliego, C., Bruno, F., Del Buono, R., Costa, F., et al. Nature 590, 635641. Perplexingly, successful balance of lung humoral metabolism may lead to the reduction of the number of COVID-19 death limiting the possibility of healthcare services with insufficient capacity to provide ventilator-assisted respiration. 21, 97S107S. medRxiv. Systems Pharmacological Study Illustrates the Immune Regulation, Anti-infection, Anti-inflammation, and Multi-Organ protection Mechanism of Qing-Fei-Pai-Du Decoction in the Treatment of COVID-19. It has already been shown that the dysregulated release of cytokines is one of the key factors behind poor outcomes in COVID-19 patients. The University of Connecticut Foundation, Inc. Office of Development and Alumni Relations 10 Talcott Notch Road Suite 100 Farmington, CT 06032 Biophys. 388 (4), 421436. (2009). Crit. TRPA1 Agonists Evoke Coughing in guinea Pig and Human Volunteers. A vision of coronavirus with the minimal set of structural proteins. Lung Injury in COVID-19 Has Pulmonary Edema as an Important Component and Treatment with Furosemide and Negative Fluid Balance (NEGBAL) Decreases Mortality. Sci. J. Biol. Care Med. 308 (11), L1136L1144. The combination of the two can lead to pneumonia and other serious respiratory illnesses. Maresin1 Stimulates Alveolar Fluid Clearance through the Alveolar Epithelial Sodium Channel Na,K-ATPase via the ALX/PI3K/Nedd4-2 Pathway. (2020c). Association between Early Treatment with Qingfei Paidu Decoction and Favorable Clinical Outcomes in Patients with COVID-19: A Retrospective Multicenter Cohort Study. Emodin Blocks the SARS Coronavirus Spike Protein and Angiotensin-Converting Enzyme 2 Interaction. 10.1111/nyas.14472 Sci. Physiol. doi:10.1007/s00424-018-2232-y, Woods, P. S., Tazi, M. F., Chesarino, N. M., Amer, A. O., and Davis, I. C. (2015). doi:10.1101/2020.02.13.20022673, Alvarez, D. F., King, J. Am. When there, the virus itself and virus-mediated protein-protein interactions lead to the lung inflammatory storm responsible for the observed increasing vascular permeability in lung and pulmonary edema (Tang et al., 2020). Furosemide, a NKCC inhibitor, has been acknowledged as first-line therapeutic drug for pulmonary edema all the time (Pickkers et al., 1997; Solymosi et al., 2013). Physiol. 158, 104850. doi:10.1016/j.phrs.2020.104850, Ma, Q., Qiu, M., Zhou, H., Chen, J., Yang, X., Deng, Z., et al. doi:10.1016/j.idc.2019.07.001, Imai, Y., Kuba, K., and Penninger, J. M. (2007). (2020). Currently, many clinical trials are in progress to test coronavirus treatment, including new drugs and drug repurposing or repositioning. Adipose-derived Exosomes Protect the Pulmonary Endothelial Barrier in Ventilator-Induced Lung Injury by Inhibiting the TRPV4/Ca2+ Signaling Pathway. 2022 Dec;134:102427. doi: 10.1016/j.artmed.2022.102427. (2014). doi:10.1055/s-0040-1712960, Deng, J., Wang, D.-x., Deng, W., Li, C.-y., Tong, J., and Ma, H. (2012). doi:10.1152/ajplung.1998.274.2.l203, Negrini, D., Passi, A., de Luca, G., and Miserocchi, G. (1996). These supportive approaches have been shown to be beneficial as adjuvant therapies in COVID-19 patients. Med. Front. doi:10.1016/j.bbagen.2005.09.009, Zhuo, X.-J., Hao, Y., Cao, F., Yan, S.-F., Li, H., Wang, Q., et al. COVID-19 mortality is primarily driven by abnormal alveolar fluid metabolism of the lung, leading to fluid accumulation in the alveolar airspace. Pharmacol. doi:10.1016/j.cell.2020.02.058, Wang, D., Hu, B., Hu, C., Zhu, F., Liu, X., Zhang, J., et al. J. Med. The Clinical Benefits of Chinese Patent Medicines against COVID-19 Based on Current Evidence. It has been reported that infection with a respiratory-associated virus can significantly increase the expression and activity of TRPV1 (Abdullah et al., 2014). This site needs JavaScript to work properly. 158 (6), 16211628. National Library of Medicine Ijerph 17 (15), 5320. doi:10.3390/ijerph17155320, Kunzelmann, K., Beesley, A. H., King, N. J., Karupiah, G., Young, J. Immunol. doi:10.1021/acsnano.0c02624, Walls, A. C., Park, Y.-J., Tortorici, M. A., Wall, A., McGuire, A. T., and Veesler, D. (2020). COVID-19 Infection: the Perspectives on Immune Responses. CT images of COVID-19 patients revealed fluid and clear liquid jelly in their lungs, both closely linked to HA (Xu et al., 2020; Wang et al., 2020). Acute Respiratory Distress Syndrome Leads to Reduced Ratio of ACE/ACE2 Activities and Is Prevented by Angiotensin-(1-7) or an Angiotensin II Receptor Antagonist. Am. COVID-19 mortality is primarily driven by abnormal alveolar fluid metabolism of the lung, leading to fluid accumulation in the alveolar airspace. medRxiv.doi:10.1101/2020.05.20.20107607, Hu, K., Guan, W.-j., Bi, Y., Zhang, W., Li, L., Zhang, B., et al. Dis. Molecular Features of Non-selective Small Molecule Antagonists of the Bradykinin Receptors. doi:10.4049/jimmunol.1302421. J. Endocrinol. Physiol. Decreased Expression of Aquaporin-5 in Bleomycin-Induced Lung Fibrosis in the Mouse fibrosis in the Mouse. In these patients, white blood cells count, neutrophil count and D-dimer level keep rising while lymphocyte count keeps decreasing as the disease progresses. (1977). 382 (18), 17081720. doi:10.1152/ajplung.1998.275.3.L631, Perkins, G. D., McAuley, D. F., Thickett, D. R., and Gao, F. (2006). Infection and replication process of SARS-CoV-2. doi:10.1002/jmv.25848, Cutts, S., Talboys, R., Paspula, C., Prempeh, E., Fanous, R., and Ail, D. (2017). This buildup of fluid leads to shortness of breath. doi:10.1056/NEJMoa2028836, Tang, Y., Liu, J., Zhang, D., Xu, Z., Ji, J., and Wen, C. (2020). The Origin, Transmission and Clinical Therapies on Coronavirus Disease 2019 (COVID-19) Outbreak - an Update on the Status. (2020). Br. 6, 331345. Certain vaccine-preventable diseases can also increase swelling of your airways and lungs. doi:10.1016/s2213-2600(20)30079-5, Yang, Y., Islam, M. S., Wang, J., Li, Y., and Chen, X. Cepharanthine, a bisbenzylisoquinoline alkaloid derived from tubers of Stephania Japonica, was shown to have a wide-spectrum inhibitor of pan--coronavirus (Fan et al., 2020; Rogosnitzky et al., 2020). COPD and asthma cause your airways to swell and become blocked with mucus, which can make it hard to breathe. As the infection progresses, the immune function is impaired, causing damage to multiple organs, additional complications, and eventually death (Yang et al., 2020). Protein Chem. TRPV1, expressed in C-fibers of the vagus nerves innervating airways (Cui et al., 2016), has been considered to play a key role in cough reflex and increased airway sensitivity caused by various diseases (Andr et al., 2009; Couto et al., 2013). Pulmonary Edema in COVID-19: Explained by Bradykinin?. Virol. doi:10.1016/bs.apcsb.2015.11.005, Cure, E., and Cumhur Cure, M. (2020). Cmp 6 (1), 1327. Physiol. However, clinical evidence showing that glucocorticoids can reduce pulmonary edema by regulating fluid absorption in alveolar and glucocorticoids is missing. As Towne et al., (2001) reported, AQP-5 expression significantly declined during pulmonary inflammation and edema, and TNF- decreased AQP5 mRNA and protein expression levels via TNFR1 and NF-B pathway (Towne et al., 2001). - Eur. Liu Shen Capsule Shows Antiviral and Anti-inflammatory Abilities against Novel Coronavirus SARS-CoV-2 via Suppression of NF-b Signaling Pathway. Physiol. Am. A recent review has summarized the effects of TRPs in pulmonary chemical injuries, which includes the representative TRPA1, TRPV1 and TRPV4 antagonists which have participated in preclinical and clinical studies (Achanta and Jordt, 2020) (Supplementary Tables S1S3). Prc, N. H. C. o. t. (2020). These in turn, lead to severe lung damage in COVID-19 patients. (2013). Pharmaceuticals 13 (9), 259. doi:10.3390/ph13090259, Ren, J.-l., Zhang, A.-H., and Wang, X.-J. doi:10.4268/cjcmm20152124, Wang, Q., Zheng, X., Cheng, Y., Zhang, Y.-L., Wen, H.-X., Tao, Z., et al. 8 (8), 807815. Phytomedicine 85, 153315. doi:10.1016/j.phymed.2020.153315, Zhou, Z., Wang, S.-Q., Liu, Y., and Miao, A.-D. (2006). Bradykinin (BK) is an important cellular mediator that causes vasodilatation and leaky blood vessels, leading to vascular leakage and edema (de Maat et al., 2020). 313 (5), L845L858. J. Respir. annals 99 (1), 1216. doi:10.1016/j.jinf.2020.02.017, Xu, Z., Shi, L., Wang, Y., Zhang, J., Huang, L., Zhang, C., et al. Structure, Function, and Evolution of Coronavirus Spike Proteins. doi:10.1016/j.resp.2011.11.009, Fan, H.-H., Wang, L.-Q., Liu, W.-L., An, X.-P., Liu, Z.-D., He, X.-Q., et al. Researches proved that SARS-CoV-2 can directly infect human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) as well as an engineered heart tissue (EHT), in cellular and organ level respectively, suggesting that the virus can replicate rapidly in the cardiomyocytes, infecting other cardiomyocytes, contributing to cardiomyocyte cell death, myocardial inflammation and even heart failure (Sharma et al., 2020; Bailey et al., 2021). Am. doi:10.1001/jama.2020.6775, Rogosnitzky, M., Okediji, P., and Koman, I. Pulmonary edema is the disequilibrium between formation and reflux of lung tissue fluid leading to the absorption of massive tissue fluid by lung lymph and vein failure. 2020 Jul;57:102833. doi: 10.1016/j.ebiom.2020.102833. doi:10.1152/physrev.1974.54.3.678, Steinritz, D., Stenger, B., Dietrich, A., Gudermann, T., and Popp, T. (2018). J. Infect. Diagn Pathol. ACIP reviews data. (2015). (2020). 99 (9), 988995. During the infection of SARS-CoV-2, RAS, BK and hyaluronic acid (HA) are all involved in the regulation of AFC and the formation of pulmonary edema (Garvin et al., 2020). Therefore, severe infections, which are induced by influenza virus, target the distal lung epithelial cells, inhibit the ENaC via activating protein kinase C (Kunzelmann et al., 2000), and damage the pulmonary surfactant (Hofer et al., 2015; Ito et al., 2015; Woods et al., 2015). Clin. For instance, angiotensin II (Ang II) can typically generate vasoconstriction and sodium retention when binding to the AGTR1 receptor and vice versa via the AGTR2 receptor (Garvin et al., 2020). Perplexingly, successful balance of lung humoral metabolism may lead to the reduction of the number of COVID-19 death limiting the possibility of healthcare services with insufficient capacity to provide ventilator-assisted respiration. -, Ai J.-W., Zhang H.-C., Xu T., Wu J., Zhu M., Yu Y.-Q., et al. (2004). DOI: 10.7759/cureus.27408 Abstract Myocarditis is one of the complications reported with COVID-19 vaccines, particularly both Pfizer-BioNTech and Moderna vaccines. Invest. Pharmacol. J. Physiology-Lung Cell Mol. 291 (6), L1207L1219. We also obtain PFTs in recovering COVID-19 patients with severe pulmonary involvement or COVID-19-related ARDS, which applies to many patients who required hospitalization. 2020. B., et al. For patients recovering from COVID-19 who have persistent, progressive, or new respiratory symptoms, we obtain PFTs including spirometry, lung volumes, and diffusion capacity. Further studies may determine if CD44 inhibitors can be of use to in COVID-19. The activities of the molecules in RAS are ruled by dynamic changes responding to an injury. Chloride Transport-Driven Alveolar Fluid Secretion Is a Major Contributor to Cardiogenic Lung Edema. doi:10.1152/ajpheart.1996.270.6.h2000, Negrini, D., Passi, A., and Moriondo, A. Received: 05 February 2021; Accepted: 25 May 2021;Published: 07 June 2021. TABLE 3. Exuberant Elevation of IP-10, MCP-3 and IL-1ra during SARS-CoV-2 Infection Is Associated with Disease Severity and Fatal Outcome. Allergol. Here, we provide a perspective on abnormal lung humoral metabolism of pulmonary edema in COVID-19 patients, review the mechanisms by which pulmonary edema may be induced in COVID-19 patients, and propose putative drug targets that may be of use in treating COVID-19. doi:10.1101/2020.03.31.20038935, Yang, R., Liu, H., Bai, C., Wang, Y., Zhang, X., Guo, R., et al. Pulmonary Interstitial Pressure and Proteoglycans during Development of Pulmonary Edema. Among all vaccine recipients, 66.6% reported at least one systemic reaction in the 7 days after vaccination. Rev. Int. J. Ethnopharmacology 265, 113301. doi:10.1016/j.jep.2020.113301, Li, F. (2016). Recombinant ACE2 was also reported to be a potential therapy in the clinical study of ARDS, which can lead to rapid decrease of plasma Ang II level and IL-6 expression. Acad. Natl. However, preliminary reports showed that some ACE inhibitors and ARBs have no significant clinical benefits in treating COVID-19 (Richardson et al., 2020), while others showed protective effects among patients with pre-existing hypertension (Yang et al., 2020; Liu et al., 2020). Cell 181 (2), 281292. Am J Physiol Lung Cell Mol Physiol. TRPs in Tox: Involvement of Transient Receptor Potential-Channels in Chemical-Induced Organ Toxicity-A Structured Review. As such, TRPV4 inhibition likely has protective and beneficial effect on mucus clearance and pulmonary edema. COVID-19, an infectious disease caused by a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has a global reach. A health care provider monitors the oxygen level. Therefore, the infection along with the rapid replication of SARS-CoV-2 causes a large amount of body fluid permeating through pulmonary alveoli, leading to ADRS. We argue for expeditious clinical testing of this inhibitor in COVID-19 patients with respiratory malfunction and at risk for lung edema. In March 2020, the World Health Organization (WHO) declared Coronavirus Disease 2019 (COVID-19) a pandemic, therefore the efforts of scientists around the world are focused on finding the right treatment and vaccine for the novel disease. Moreover, the peripheral blood mononuclear lymphocyte of COVID-19 patients was also greatly improved, from 0.91 0.54 to 1.24 0.67 after being treated for a week, while there was no obvious change in control group (Hu et al., 2020). 346, 16311636. J. Med. Sci. J. Respir. Moreover, other drugs which can regulate immune system like hydroxychloroquine and azithromycin may also show effects in treating SARS-COV-2-induced pulmonary edema and their effectiveness in treating SARS-COV-2 infections should be further investigated. 11. The https:// ensures that you are connecting to the It has been observed that MMP-2 and MMP-9, two most crucial MMPs in the lung are over-expressed in pulmonary edema (Negrini et al., 1996; Negrini et al., 1998; Passi et al., 1998), suggesting that MMPs may become a potential target for pulmonary edema treatment. Hyponatremia in Infectious Diseases-A Literature Review. N.Y. Acad. 10.5582/ddt.2020.03070 Pharmacol. In addition, potassium channels can act as oxygen sensors in alveolar epithelium and thus adjust lung function to environmental changes in O2 levels (Bartoszewski et al., 2017). The general regulation approaches of AFC. A type of pulmonary edema called neurogenic pulmonary edema can occur after a head injury, seizure or brain . Contact. Thus, it could be a potential RdRp inhibitor for SARS-CoV-2 (Lung et al., 2020). 2, 1019. Clin. It is known that SARS-CoV-2 invades human cells by binding angiotensin-converting enzyme-2 (ACE-2) receptor and other membrane ectopeptidases (Xu et al., 2020). Studies showed that ENaC activators or stimulators can regulate ENaC-dependent fluid absorption in alveolar and pulmonary edema (Fronius, 2013). Med. Thorax 69 (1), 4654. These channels are important in maintaining the optimum volume and ion constitution of bronchial periciliary fluid and alveolar lining fluid layers, which are necessary in appropriate pathogens mucociliary clearance and optimum gas exchange, respectively (Londino et al., 2017). 54 (10), 774780. doi:10.1056/NEJMoa013183, Sayegh, R., Auerbach, S. D., Li, X., Loftus, R. W., Husted, R. F., Stokes, J. Rep. 72 (6), 15091516. COVID-19 Vaccine: A Comprehensive Status Report. After getting vaccinated for COVID-19, you might experience some temporary symptoms similar to those you might notice when you get a flu shot, such as a sore, swollen arm where you got the shot. Xue-Bi-Jing injection is also widely applicated in treating COVID-19 patients and by adding it based on the routine anti-infective therapy, the 28-day mortality of patients with severe pneumonia could be reduced by 8.8%, greatly improving pneumonia severity index (from 93.18 23.17 to 52.18 30.53) (Ma et al., 2020b). Immunol. Epub 2023 Mar 31. Digestive System Is a Potential Route of COVID-19: an Analysis of Single-Cell Coexpression Pattern of Key Proteins in Viral Entry Process. (2020c). doi:10.1161/CIRCRESAHA.107.168724, Yin, J., Michalick, L., Tang, C., Tabuchi, A., Goldenberg, N., Dan, Q., et al. doi:10.1111/nyas.14472, Adil, M. S., Narayanan, S. P., and Somanath, P. R. (2020). (2014). Medicines 16 (11), 811828. Dis. A., et al. COVID-19 can cause lung complications such as pneumonia and, in the most severe cases, acute respiratory distress syndrome, or ARDS . and transmitted securely. N. Engl. Jiangsu Qing Lan Project for Young Academic Leaders of China. Efficacy of Tocilizumab in Patients Hospitalized with Covid-19. (2019). First post-authorization U.S. doses of Janssen COVID -19 Vaccine. Moreover, as a retrospective multicenter cohort study reported, early treatment with Qing-Fei-Pai-Du Decoction associated with better outcomes, faster recovery, and a shorter duration of hospital stay (Shi et al., 2020a). Optimizing Diagnostic Strategy for Novel Coronavirus Pneumonia, a Multi-center Study in Eastern China. doi:10.1111/joim.13091, Passi, A., Negrini, D., Albertini, R., de Luca, G., and Miserocchi, G. (1998). 7 (4). 2, 26372646. Pharmacol. Pharmacol. Pathological Findings of COVID-19 Associated with Acute Respiratory Distress Syndrome. (2020a). (Engl) 133 (9), 10511056. Int. Cough Reflex Testing with Inhaled Capsaicin and TRPV1 Activation in Asthma and Comorbid Conditions. Abnormal humoral metabolism is mainly manifested as imbalances of water and electrolytes. Chin. Wiersinga, W. J., Rhodes, A., Cheng, A. C., Peacock, S. J., and Prescott, H. C. (2020). Intensive Care Med. (2020). Anti-hypertensive Angiotensin II Receptor Blockers Associated to Mitigation of Disease Severity in Elderly COVID-19 Patients. Diagnosing COVID-19: The Disease and Tools for Detection. Accessibility (2020). Pulmonary capillary leak syndrome following COVID-19 virus infection. Additionally, other major ADRs were potentially linked to the BNT162b2 mRNA COVID-19 vaccine, including central nervous system thrombosis, deep vein thrombosis, and pulmonary embolism [3-5]. Federal government websites often end in .gov or .mil. The project supported by Natural Science Foundation of China (grant number 81673563, 81102762, and 81274199); Open Project Program of Jiangsu Collaborative Innovation Center of Chinese Medicinal Resources Industrialization (ZDXM-1-14, FJGJS-2015-15); Fund of Quality Standardization of Liu-Shen-Wan (BA2016104, ZYBZH-C-JS-30). The Supplementary Material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fphar.2021.664349/full#supplementary-material, Abdullah, H., Heaney, L. G., Cosby, S. L., and McGarvey, L. P. A. J. One day before symptom onset, he had received a COVID-19 mRNA vaccine. Artif Intell Med. Chloroquine and Hydroxychloroquine in Covid-19. Alternative Names Lung congestion; Lung water; Pulmonary congestion; Heart failure - pulmonary edema Causes Pulmonary edema is often caused by congestive heart failure. Impaired Breakdown of Bradykinin and its Metabolites as a Possible Cause for Pulmonary Edema in COVID-19 Infection. Neurobiol. Thus, promoting the degradation of HA may be significant in the recovery process. The structure of coronavirus (Figure 1 A vision of coronavirus with the minimal set of structural proteins.) Therefore, the S protein determines the host cell of the virus, regulates the viral attachment and fusion with the host cell membrane, and promotes cellular invasion. North America 33 (4), 869889. N.Y. Acad. Physiol. 289 (1), L104L110. Adult Respiratory Distress Syndrome. (2013). These cytokine storms can be treated with steroids, IL-1 antagonists, TNF inhibitors, and Janus kinase inhibitor (JAK) inhibitors (McCreary and Pogue, 2020). 110 (25), E2308E2316. Available: https://covid19.who.int/ (Accessed March 31, 2021). doi:10.1136/thoraxjnl-2013-203894, PubMed Abstract | CrossRef Full Text | Google Scholar, Achanta, S., and Jordt, S. E. (2020). TRPV4: Physiological Role and Therapeutic Potential in Respiratory Diseases. J. Pathol. doi:10.1161/01.RES.0000247065.11756.19, Andr, E., Gatti, R., Trevisani, M., Preti, D., Baraldi, P., Patacchini, R., et al. doi:10.1002/jcp.28602, Otulakowski, G., Rafii, B., Bremner, H. R., and O'Brodovich, H. (1999). J. Nat. J. Biol. Immune-modulatory agents for COVID-19 include tocilizumab, human immunoglobulin and the convalescent plasma. In December 2019, a novel coronavirus, SARS-CoV-2, appeared, causing a wide range of symptoms, mainly respiratory infection. Theaflavin from black tea was found to present a lower binding energy when it docks in the catalytic pocket of SARS-CoV-2 RdRp. Glucocorticoids were shown to have the ability of inducing de novo synthesis of ENaC (Chow et al., 1999; Otulakowski et al., 1999; Sayegh et al., 1999) and affecting ENaC regulatory pathway via serum and glucocorticoids-inducible kinase-1 (SGK-1) (Chen et al., 1999; de la Rosa et al., 1999; Itani et al., 2001; Zhang et al., 2007). Impact of -adrenergic Agonist on Na+ Channel and Na+-K+-ATPase Expression in Alveolar Type II Cells. Circ. The first treatment for acute pulmonary edema is oxygen. Blood 135 (23), 20332040. (2020). Br. The frequency and severity of systemic adverse events was higher after dose 2 than dose 1. Physiol. Not everyone gets side effects. -. Patients receive high-flow nasal cannula (HFNC), non-invasive ventilation (NIV), mechanical ventilation or ECMO as respiratory supports (Guo et al., 2020; Pascarella et al., 2020), a crystalloid fluid to ensure body fluid equilibrium (Christ-Crain et al., 2020), and anticoagulants for restraining the thrombus formation to aid in circulatory support (Connors and Levy, 2020). Res. Toxicol. doi:10.1152/ajplung.00395.2015, Birrell, M. A., Belvisi, M. G., Grace, M., Sadofsky, L., Faruqi, S., Hele, D. J., et al. Res. Physiology 23, 360370. 1480 (1), 73103. doi:10.1002/jmv.25761, Luo, X., Ni, X., Lin, J., Zhang, Y., Wu, L., Huang, D., et al. TRPs are essential for the respiratory system and pulmonary edema, in which TRPA1, TRPV1 and TRPV4 are the most important. Thus, the relieve of pulmonary edema should be one of the critical concerns in terms of the treatment of COVID-19 patients. 19 (5), 305306. TALLAHASSEE, Fla. Florida Surgeon General Joseph Ladapo personally altered a state-driven study about Covid-19 vaccines last year to suggest that some doses pose a . Virol. doi:10.1177/0004563220922255, Liu, Y., Huang, F., Xu, J., Yang, P., Qin, Y., Cao, M., et al. Mechanism of inhibiting ENaC inducing pulmonary edema. A Mechanistic Model and Therapeutic Interventions for COVID-19 Involving a RAS-Mediated Bradykinin Storm. Quantitative mRNA Expression Profiling of ACE 2, a Novel Homologue of Angiotensin Converting Enzyme. doi:10.1136/bmj.m1432, Fleckenstein, A. Infection and replication process of SARS-CoV-2. There are multiple potential mechanisms leading to pulmonary edema in severe Coronavirus Disease (COVID-19) patients and understanding of those mechanisms may enable proper management of this condition. 46 (7), 835837. Oxygen flows through a face mask or a flexible plastic tube with two openings (nasal cannula) that deliver oxygen to each nostril. 180 (11), 10421047. The latest research revealed that alveolar macrophages, which normally play a protective role, may also be infected by SARS-CoV-2 and release T cell chemokines, resulting large amounts of T cells gathering in lung and generating IFN. (1999). 2021 Jun 7;12:664349. doi: 10.3389/fphar.2021.664349. Atractylenolide I Inhibits Lipopolysaccharide-Induced Inflammatory Responses via Mitogen-Activated Protein Kinase Pathways in RAW264.7 Cells. doi: 10.1152/ajplung.00161.2020. Bookshelf 157, 104820. doi:10.1016/j.phrs.2020.104820, Yang, X., Yu, Y., Xu, J., Shu, H., Xia, J. a., Liu, H., et al. (2020). However, as we discussed above, the inhibition of ENaC can also induce pulmonary edema and further studies are required to determine the potential use of ENaC inhibitors for COVID-19 treatment. A., and Cook, D. I. (2020a). J. Appl. Currently, these symptoms are the primary consequences of pulmonary virus infection. (1998). Respir. There are also several natural compounds which were previously shown to have positive effects on the lung edema-associated targets described in this paper (Zhou et al., 2006; Ho et al., 2007; Ji et al., 2014; Wang et al., 2015; Qu, 2019; Fan et al., 2020; Lung et al., 2020). K+ Channels Regulate ENaC Expression via Changes in Promoter Activity and Control Fluid Clearance in Alveolar Epithelial Cells. An Orally Active TRPV4 Channel Blocker Prevents and Resolves Pulmonary Edema Induced by Heart Failure. Neurosci. Rhinovirus Upregulates Transient Receptor Potential Channels in a Human Neuronal Cell Line: Implications for Respiratory Virus-Induced Cough Reflex Sensitivity. Here, we describe molecular mechanisms of PFC and propose that proteins functioning in this process might serve as an underappreciated, but yet promising targets for reducing lung edema in severe COVID-19 patients. Inhibiting these TRPs may benefit the treatment of pulmonary edema. Sharma, A., Garcia, G., Wang, Y., Plummer, J. T., Morizono, K., Arumugaswami, V., et al. Yes. doi:10.1007/s11596-015-1490-6, Jovanovi, S., Crawford, R. M., Ranki, H. J., and Jovanovi, A. Res. HHS Vulnerability Disclosure, Help 276 (22), 1865718664. Large Conductance Ca2+-Activated K+ Channels Sense Acute Changes in Oxygen Tension in Alveolar Epithelial Cells. doi:10.1111/bph.12414, Kaur, S. P., and Gupta, V. (2020). The condition presents itself as a slowly evolving pneumonia with insidious early onset interstitial pulmonary edema that undergoes acute exacerbation in the late stages and alveolar edema (Xu et al., 2020; Wiersinga et al., 2020). Epithelial sodium channel (ENaC), present in human lungs, kidneys and other organs, plays a vital role in lung fluid clearance (Figure 4 Mechanism of inhibiting ENaC inducing pulmonary edema) (Matthay et al., 2002). Technol. Focusing on decreasing the formation of body fluid in lung or promoting the absorption of body fluid can contribute to a decrease in lung damage and decreased mortality in COVID-19 patients. Am. doi:10.1007/s42399-020-00610-8, Ai, J.-W., Zhang, H.-C., Xu, T., Wu, J., Zhu, M., Yu, Y.-Q., et al. doi:10.1172/JCI29850, Zhao, J., Tian, S., Lu, D., Yang, J., Zeng, H., Zhang, F., et al. DD&T 14 (5), 256258. (2017). Millions of people in the United States have received COVID-19 vaccines and they are safe and effective at protecting against COVID-19. As of Sunday, at least 16,183 people had filed complaints with the Centers for Disease Control and Prevention that they'd developed tinnitus, or ringing in their ears, after receiving a Covid vaccine. doi:10.1161/01.RES.0000125623.56442.20, Nayler, W., and Dillon, J. Careers. Some natural compounds along with their antiviral and reducing pulmonary edema mechanisms are shown in Table 2. As Gabazza et al., (2004) reported, lung fibrosis is linked to decreased mRNA and protein expression of AQP-5 in the lung. Nervous system conditions or surgeries. J. Respir. (2020). Remdesivir for the Treatment of Covid-19 - Final Report. Vaccines (Basel). 383 (19), 18131826. J. Med. Unauthorized use of these marks is strictly prohibited. (2020). TGF--induced IL-6 prevents development of acute lung injury in influenza A virus-infected F508del CFTR-heterozygous mice. Patients with SARS-CoV-2-Induced Viral Sepsis Simultaneously Show Immune Activation, Impaired Immune Function and a Procoagulatory Disease State. Potentially, glucocorticoids can be used as anti-inflammatory drugs in ARDS and pulmonary edema as well as in COVID-19 patients. When SARS-COV-2 invades, vascular endothelial cells are damaged, causing insufficient arterial flow and minimal thrombus. Phytomedicine 85, 153282. doi:10.1016/j.phymed.2020.153282, Ma, Q., Pan, W., Li, R., Liu, B., Li, C., Xie, Y., et al. A blocked upper airway causes negative pressure in the lungs from trying to breathe through the blockage. Lancet Respir. doi:10.1101/2020.03.02.20029975, Yin, J., Hoffmann, J., Kaestle, S. M., Neye, N., Wang, L., Baeurle, J., et al. This condition is generally referred to as pulmonary edema and is a direct consequence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.

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