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=== Relationship to COVID-19===
=== Relationship to COVID-19===
During the [[COVID-19 pandemic]], some doctors attributed many deaths to cytokine storms.<ref name="covid-3">{{cite journal | vauthors = Mehta P, McAuley DF, Brown M, Sanchez E, Tattersall RS, Manson JJ | title = COVID-19: consider cytokine storm syndromes and immunosuppression | journal = Lancet | volume = 395 | issue = 10229 | pages = 1033–1034 | date = March 2020 | pmid = 32192578 | doi = 10.1016/S0140-6736(20)30628-0 | pmc = 7270045 | doi-access = free }}</ref><ref name="covid-2">{{cite journal | vauthors = Ruan Q, Yang K, Wang W, Jiang L, Song J | title = Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China | journal = Intensive Care Medicine | date = March 2020 | volume = 46 | issue = 5 | pages = 846–848 | pmid = 32125452 | pmc = 7080116 | doi = 10.1007/s00134-020-05991-x }}</ref>
During the [[COVID-19 pandemic]], some doctors attributed many deaths to cytokine storms.<ref name="covid-3">{{cite journal | vauthors = Mehta P, McAuley DF, Brown M, Sanchez E, Tattersall RS, Manson JJ | title = COVID-19: consider cytokine storm syndromes and immunosuppression | journal = Lancet | volume = 395 | issue = 10229 | pages = 1033–1034 | date = March 2020 | pmid = 32192578 | doi = 10.1016/S0140-6736(20)30628-0 | pmc = 7270045 | doi-access = free }}</ref><ref name="covid-2">{{cite journal | vauthors = Ruan Q, Yang K, Wang W, Jiang L, Song J | title = Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China | journal = Intensive Care Medicine | date = March 2020 | volume = 46 | issue = 5 | pages = 846–848 | pmid = 32125452 | pmc = 7080116 | doi = 10.1007/s00134-020-05991-x }}</ref>
The higher mortality is being linked to the result of ARDS aggravation and the tissue damage that can result in organ-failure and/or death.<ref name="doi.org">{{cite journal |last1=Ragad |first1=Dina |title=The COVID-19 Cytokine Storm; What we know so far |journal=Front. Immunol |date=16 June 2020 |url=https://doi.org/10.3389/fimmu.2020.01446}}</ref> In a cytokine plasma level analysis of those with severe Sars-CoV-2, the levels of many interleukins and cytokines are extremely elevated, showing evidence of a cytokine storm in those most harshly affected.<ref name="doi.org"/> Early recognition of this cytokine storm in COVID-19 patients is crucial to ensure the best outcome, allowing for treatment with a variety of biological agents that target the cytokines to reduce their levels. Due to the increased levels of cytokines and interferons in those with severe Sars-CoV-2, both are being investigated as a potential therapy for COVID-19.
The higher mortality is being linked to the result of ARDS aggravation and the tissue damage that can result in organ-failure and/or death.<ref name="doi.org">{{cite journal |last1=Ragad |first1=Dina |title=The COVID-19 Cytokine Storm; What we know so far |journal=Front. Immunol |date=16 June 2020 |url=https://doi.org/10.3389/fimmu.2020.01446}}</ref> In a cytokine plasma level analysis of those with severe Sars-CoV-2, the levels of many interleukins and cytokines are extremely elevated, showing evidence of a cytokine storm in those most harshly affected.<ref name="doi.org"/> Additionally, postmortem examination of patients with COVID-19 has shown large accumulation of inflammatory cells in lung tissues, including macrophages and T-helper cells.<ref>{{Cite journal|last=Tang|first=Yujun|last2=Liu|first2=Jiajia|last3=Zhang|first3=Dingyi|last4=Xu|first4=Zhenghao|last5=Ji|first5=Jinjun|last6=Wen|first6=Chengping|date=2020-07-10|title=Cytokine Storm in COVID-19: The Current Evidence and Treatment Strategies|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7365923/|journal=Frontiers in Immunology|volume=11|doi=10.3389/fimmu.2020.01708|issn=1664-3224|pmc=7365923|pmid=32754163}}</ref> Early recognition of this cytokine storm in COVID-19 patients is crucial to ensure the best outcome, allowing for treatment with a variety of biological agents that target the cytokines to reduce their levels. Due to the increased levels of cytokines and interferons in those with severe Sars-CoV-2, both are being investigated as a potential therapy for COVID-19.
A [https://link.springer.com/article/10.1007/s00281-017-0629-x?fbclid=IwAR0xBnmDapKpJn8lryYFoWbhzorGXqxcB9lN1zfWWaM6jrMfizSzWrU1ZAs&error=cookies_not_supported&code=8cdcb8b4-169b-461e-ad03-b1a6c16a3db9.html study] by Stanley Perlman, a University of Iowa professor, cited in the [https://www.nytimes.com/2020/08/11/magazine/covid-cytokine-storms.html New York Times] done on mice found that those that could produce strong interferon responses to SARS-CoV, which also originated from bats, ''early'' would be more likely to live; otherwise, they would see an overactive immune system that would spell doom. As humans age, we have an increasingly difficult time building a timely, adequate interferon response, which may explain why mortality rates are greater in older populations.
A [https://link.springer.com/article/10.1007/s00281-017-0629-x?fbclid=IwAR0xBnmDapKpJn8lryYFoWbhzorGXqxcB9lN1zfWWaM6jrMfizSzWrU1ZAs&error=cookies_not_supported&code=8cdcb8b4-169b-461e-ad03-b1a6c16a3db9.html study] by Stanley Perlman, a University of Iowa professor, cited in the [https://www.nytimes.com/2020/08/11/magazine/covid-cytokine-storms.html New York Times] done on mice found that those that could produce strong interferon responses to SARS-CoV, which also originated from bats, ''early'' would be more likely to live; otherwise, they would see an overactive immune system that would spell doom. As humans age, we have an increasingly difficult time building a timely, adequate interferon response, which may explain why mortality rates are greater in older populations.


Revision as of 03:35, 4 December 2020

Not to be confused with Cytokine release syndrome.

A cytokine storm, also called hypercytokinemia, is a physiological reaction in humans and other animals in which the innate immune system causes an uncontrolled and excessive release of pro-inflammatory signaling molecules called cytokines. Normally, cytokines are part of the body's immune response to infection, but their sudden release in large quantities can cause multisystem organ failure and death.[1] Cytokine storms can be caused by a number of infectious and non-infectious etiologies, especially viral respiratory infections such as H5N1 influenza, SARS-CoV-1,[2][3] and SARS-CoV-2 (COVID-19 agent). Other causative agents include the Epstein-Barr virus, cytomegalovirus, and group A streptococcus, and non-infectious conditions such as graft-versus-host disease.[4] The viruses can invade lung epithelial cells and alveolar macrophages to produce viral nucleic acid, which stimulates the infected cells to release cytokines and chemokines, activating macrophages, dendritic cells, and others.[5]

Cytokine storm syndrome is diverse set of conditions that can result in cytokine storm. Cytokine storm syndromes include familiar hemophagocytic lymphohistiocytosis, Epstein-Barr virus–associated hemophagocytic lymphohistiocytosis, systemic or non-systemic juvenile idiopathic arthritis–associated macrophage activation syndrome, NLRC4 macrophage activation syndrome, cytokine release syndrome and sepsis.[6]

Cytokine storms versus cytokine release syndrome

The term "cytokine storm" is often loosely used interchangeably with cytokine release syndrome (CRS) but is more precisely a differentiable syndrome that may represent a severe episode of cytokine release syndrome or a component of another disease entity, such as macrophage activation syndrome. When occurring as a result of a therapy, CRS symptoms may be delayed until days or weeks after treatment. Immediate-onset (fulminant) CRS appears to be a cytokine storm.[7]

Research

Nicotinamide (a form of vitamin B3) is a potent inhibitor of proinflammatory cytokines.[8][9]

Magnesium decreases inflammatory cytokine production by modulation of the immune system.[10][11]

History

The first reference to the term cytokine storm in the published medical literature appears to be by Ferrara et al. in 1993 in a discussion of graft vs. host disease; a condition in which the role of excessive and self-perpetuating cytokine release had already been under discussion for many years.[12][13] The term next appeared in a discussion of pancreatitis in 2002, and in 2003 it was first used in reference to a reaction to an infection.[12]

It is believed that cytokine storms were responsible for the disproportionate number of healthy young adult deaths during the 1918 influenza pandemic, which killed 17 to 50 million people. In this case, a healthy immune system may have been a liability rather than an asset.[14] Preliminary research results from Taiwan also indicated this as the probable reason for many deaths during the SARS epidemic in 2003.[15] Human deaths from the bird flu H5N1 usually involve cytokine storms as well.[16] Cytokine storm has also been implicated in hantavirus pulmonary syndrome.[17]

In 2006, a study at Northwick Park Hospital in England resulted in all 6 of the volunteers given the drug theralizumab becoming critically ill, with multiple organ failure, high fever, and a systemic inflammatory response.[18][19]Parexel, a company conducting trials for pharmaceutical companies, in one of its documents, wrote about the trial and said theralizumab could cause a cytokine storm—the dangerous reaction the men experienced.[20]

Relationship to COVID-19

During the COVID-19 pandemic, some doctors attributed many deaths to cytokine storms.[21][22] The higher mortality is being linked to the result of ARDS aggravation and the tissue damage that can result in organ-failure and/or death.[23] In a cytokine plasma level analysis of those with severe Sars-CoV-2, the levels of many interleukins and cytokines are extremely elevated, showing evidence of a cytokine storm in those most harshly affected.[23] Additionally, postmortem examination of patients with COVID-19 has shown large accumulation of inflammatory cells in lung tissues, including macrophages and T-helper cells.[24] Early recognition of this cytokine storm in COVID-19 patients is crucial to ensure the best outcome, allowing for treatment with a variety of biological agents that target the cytokines to reduce their levels. Due to the increased levels of cytokines and interferons in those with severe Sars-CoV-2, both are being investigated as a potential therapy for COVID-19. A study by Stanley Perlman, a University of Iowa professor, cited in the New York Times done on mice found that those that could produce strong interferon responses to SARS-CoV, which also originated from bats, early would be more likely to live; otherwise, they would see an overactive immune system that would spell doom. As humans age, we have an increasingly difficult time building a timely, adequate interferon response, which may explain why mortality rates are greater in older populations.

Trials continue to identify causes of cytokine storms.[25][26]

Cytokine storms could arise because of different reasons, but Mangalmurti and Hunter mention in their article that “diabetes, hypertension, and cardiovascular disease” could all help to lead to cytokine storms in a body that is already fighting the novel coronavirus (Mangalmurti and Hunter, 2020, 24).[27]

References

  1. ^ Farsalinos, Konstantinos; Barbouni, Anastasia; Niaura, Raymond (2020). "Systematic review of the prevalence of current smoking among hospitalized COVID-19 patients in China: Could nicotine be a therapeutic option?". Internal and Emergency Medicine. 15 (5): 845–852. doi:10.1007/s11739-020-02355-7. PMC 7210099. PMID 32385628.
  2. ^ Wong, Jonathan P.; Viswanathan, Satya; Wang, Ming; Sun, Lun-Quan; Clark, Graeme C.; D'Elia, Riccardo V. (February 2017). "Current and future developments in the treatment of virus-induced hypercytokinemia". Future Medicinal Chemistry. 9 (2): 169–178. doi:10.4155/fmc-2016-0181. ISSN 1756-8927. PMC 7079716. PMID 28128003.
  3. ^ Liu, Qiang; Zhou, Yuan-hong; Yang, Zhan-qiu (January 2016). "The cytokine storm of severe influenza and development of immunomodulatory therapy". Cellular & Molecular Immunology. 13 (1): 3–10. doi:10.1038/cmi.2015.74. PMC 4711683. PMID 26189369.
  4. ^ Tisoncik, Jennifer R.; Korth, Marcus J.; Simmons, Cameron P.; Farrar, Jeremy; Martin, Thomas R.; Katze, Michael G. (2012). "Into the Eye of the Cytokine Storm". Microbiology and Molecular Biology Reviews. 76 (1): 16–32. doi:10.1128/MMBR.05015-11. ISSN 1092-2172. PMC 3294426. PMID 22390970.
  5. ^ Song, Peipei; Li, Wei; Xie, Jianqin; Hou, Yanlong; You, Chongge (October 2020). "Cytokine storm induced by SARS-CoV-2". Clinica Chimica Acta; International Journal of Clinical Chemistry. 509: 280–287. doi:10.1016/j.cca.2020.06.017. ISSN 0009-8981. PMC 7283076. PMID 32531256.
  6. ^ Behrens, Edward M.; Koretzky, Gary A. (2017). "Review: Cytokine Storm Syndrome: Looking Toward the Precision Medicine Era". Arthritis & Rheumatology. 69 (6): 1135–1143. doi:10.1002/art.40071. ISSN 2326-5205. PMID 28217930.
  7. ^ Porter D, Frey N, Wood PA, Weng Y, Grupp SA (March 2018). "Grading of cytokine release syndrome associated with the CAR T cell therapy tisagenlecleucel". Journal of Hematology & Oncology. 11 (1): 35. doi:10.1186/s13045-018-0571-y. PMC 5833070. PMID 29499750.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  8. ^ Ungerstedt JS, Blömback M, Söderström T (2003). "Nicotinamide is a potent inhibitor of proinflammatory cytokines". Clin Exp Immunol. 131 (1): 48–52. doi:10.1046/j.1365-2249.2003.02031.x. PMC 1808598. PMID 12519385.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  9. ^ Yanez M, Jhanji M, Murphy K, Gower RM, Sajish M, Jabbarzadeh E (2019). "Nicotinamide Augments the Anti-Inflammatory Properties of Resveratrol through PARP1 Activation". Sci Rep. 9 (1): 10219. Bibcode:2019NatSR...910219Y. doi:10.1038/s41598-019-46678-8. PMC 6629694. PMID 31308445.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  10. ^ Sugimoto J, Romani AM, Valentin-Torres AM, Luciano AA, Ramirez Kitchen CM, Funderburg N; et al. (2012). "Magnesium decreases inflammatory cytokine production: a novel innate immunomodulatory mechanism". J Immunol. 188 (12): 6338–46. doi:10.4049/jimmunol.1101765. PMC 3884513. PMID 22611240.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  11. ^ Nielsen FH (2018). "Magnesium deficiency and increased inflammation: current perspectives". J Inflamm Res. 11: 25–34. doi:10.2147/JIR.S136742. PMC 5783146. PMID 29403302.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  12. ^ a b Clark, Ian A (June 2007). "The advent of the cytokine storm". Immunology & Cell Biology. 85 (4): 271–273. doi:10.1038/sj.icb.7100062. PMID 17551531. S2CID 40463322.
  13. ^ Ferrara JL, Abhyankar S, Gilliland DG (February 1993). "Cytokine storm of graft-versus-host disease: a critical effector role for interleukin-1". Transplantation Proceedings. 25 (1 Pt 2): 1216–7. PMID 8442093.
  14. ^ Osterholm MT (May 2005). "Preparing for the next pandemic". The New England Journal of Medicine. 352 (18): 1839–42. CiteSeerX 10.1.1.608.6200. doi:10.1056/NEJMp058068. PMID 15872196.
  15. ^ Huang KJ, Su IJ, Theron M, Wu YC, Lai SK, Liu CC, Lei HY (February 2005). "An interferon-gamma-related cytokine storm in SARS patients". Journal of Medical Virology. 75 (2): 185–94. doi:10.1002/jmv.20255. PMC 7166886. PMID 15602737.
  16. ^ Haque A, Hober D, Kasper LH (October 2007). "Confronting potential influenza A (H5N1) pandemic with better vaccines". Emerging Infectious Diseases. 13 (10): 1512–8. doi:10.3201/eid1310.061262. PMC 2851514. PMID 18258000.
  17. ^ Mori M, Rothman AL, Kurane I, Montoya JM, Nolte KB, Norman JE, et al. (February 1999). "High levels of cytokine-producing cells in the lung tissues of patients with fatal hantavirus pulmonary syndrome". The Journal of Infectious Diseases. 179 (2): 295–302. doi:10.1086/314597. PMID 9878011.
  18. ^ The Lancet Oncology (February 2007). "High stakes, high risks". The Lancet. Oncology. 8 (2): 85. doi:10.1016/S1470-2045(07)70004-9. PMID 17267317.
  19. ^ Yiu, Hao Hong; Graham, Andrea L.; Stengel, Robert F. (1 October 2012). "Dynamics of a Cytokine Storm". PLOS ONE. 7 (10): e45027. Bibcode:2012PLoSO...745027Y. doi:10.1371/journal.pone.0045027. PMC 3462188. PMID 23049677.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  20. ^ Coghlan A (2006-08-14). "Mystery over drug trial debacle deepens". Health. New Scientist. Retrieved 2009-04-29.
  21. ^ Mehta P, McAuley DF, Brown M, Sanchez E, Tattersall RS, Manson JJ (March 2020). "COVID-19: consider cytokine storm syndromes and immunosuppression". Lancet. 395 (10229): 1033–1034. doi:10.1016/S0140-6736(20)30628-0. PMC 7270045. PMID 32192578.
  22. ^ Ruan Q, Yang K, Wang W, Jiang L, Song J (March 2020). "Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China". Intensive Care Medicine. 46 (5): 846–848. doi:10.1007/s00134-020-05991-x. PMC 7080116. PMID 32125452.
  23. ^ a b Ragad, Dina (16 June 2020). "The COVID-19 Cytokine Storm; What we know so far". Front. Immunol.
  24. ^ Tang, Yujun; Liu, Jiajia; Zhang, Dingyi; Xu, Zhenghao; Ji, Jinjun; Wen, Chengping (2020-07-10). "Cytokine Storm in COVID-19: The Current Evidence and Treatment Strategies". Frontiers in Immunology. 11. doi:10.3389/fimmu.2020.01708. ISSN 1664-3224. PMC 7365923. PMID 32754163.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  25. ^ Hermine, Olivier; Mariette, Xavier; Tharaux, Pierre-Louis; Resche-Rigon, Matthieu; Porcher, Raphaël; Ravaud, Philippe; CORIMUNO-19 Collaborative Group (20 October 2020). "Effect of Tocilizumab vs Usual Care in Adults Hospitalized With COVID-19 and Moderate or Severe Pneumonia: A Randomized Clinical Trial". JAMA Internal Medicine. doi:10.1001/jamainternmed.2020.6820. PMC 7577198. PMID 33080017.{{cite journal}}: CS1 maint: numeric names: authors list (link)
  26. ^ Gupta, Shruti; Wang, Wei; Hayek, Salim S.; Chan, Lili; Mathews, Kusum S.; Melamed, Michal L.; Brenner, Samantha K.; Leonberg-Yoo, Amanda; Schenck, Edward J.; Radbel, Jared; Reiser, Jochen; Bansal, Anip; Srivastava, Anand; Zhou, Yan; Finkel, Diana; Green, Adam; Mallappallil, Mary; Faugno, Anthony J.; Zhang, Jingjing; Velez, Juan Carlos Q.; Shaefi, Shahzad; Parikh, Chirag R.; Charytan, David M.; Athavale, Ambarish M.; Friedman, Allon N.; Redfern, Roberta E.; Short, Samuel A. P.; Correa, Simon; Pokharel, Kapil K.; Admon, Andrew J.; Donnelly, John P.; Gershengorn, Hayley B.; Douin, David J.; Semler, Matthew W.; Hernán, Miguel A.; Leaf, David E.; STOP-COVID Investigators (20 October 2020). "Association Between Early Treatment With Tocilizumab and Mortality Among Critically Ill Patients With COVID-19". JAMA Internal Medicine. doi:10.1001/jamainternmed.2020.6252. PMC 757720. PMID 33080002.
  27. ^ Mangalmurti, Nilam; Hunter, Christopher A. (14 July 2020). "Cytokine Storms: Understanding COVID-19". Immunity. 53 (1): 19–25 – via ScienceDirect.
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