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* Cytokine storm is an immune reaction that is characterized by dysregulated and excessive release of proinflammatory cytokines.<ref name="pmid22390970">{{cite journal| author=Tisoncik JR, Korth MJ, Simmons CP, Farrar J, Martin TR, Katze MG| title=Into the eye of the cytokine storm. | journal=Microbiol Mol Biol Rev | year= 2012 | volume= 76 | issue= 1 | pages= 16-32 | pmid=22390970 | doi=10.1128/MMBR.05015-11 | pmc=3294426 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22390970  }} </ref>
* Cytokine storm is an immune reaction that is characterized by dysregulated and excessive release of proinflammatory cytokines.<ref name="pmid22390970">{{cite journal| author=Tisoncik JR, Korth MJ, Simmons CP, Farrar J, Martin TR, Katze MG| title=Into the eye of the cytokine storm. | journal=Microbiol Mol Biol Rev | year= 2012 | volume= 76 | issue= 1 | pages= 16-32 | pmid=22390970 | doi=10.1128/MMBR.05015-11 | pmc=3294426 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22390970  }} </ref>
* During sepsis, cytokine storm may be the cause of cell or organ injury.<ref name="pmid28555385">{{cite journal| author=Chousterman BG, Swirski FK, Weber GF| title=Cytokine storm and sepsis disease pathogenesis. | journal=Semin Immunopathol | year= 2017 | volume= 39 | issue= 5 | pages= 517-528 | pmid=28555385 | doi=10.1007/s00281-017-0639-8 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28555385  }} </ref>  
* During sepsis, cytokine storm may be the cause of cell or organ injury.<ref name="pmid28555385">{{cite journal| author=Chousterman BG, Swirski FK, Weber GF| title=Cytokine storm and sepsis disease pathogenesis. | journal=Semin Immunopathol | year= 2017 | volume= 39 | issue= 5 | pages= 517-528 | pmid=28555385 | doi=10.1007/s00281-017-0639-8 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28555385  }} </ref>


=== Cytokines ===


=== Types of Cytokines ===
* Cytokines are small proteins that are released for cell signaling.<ref name="pmid22390970" />
'''Interferons  '''
* Cytokine types and their actions include:<ref name="pmid22390970" />
 
** '''Interferons''' '''(INFs)'''
*  
*** Key role in innate immunity
 
*** Regulation of the production of antiviral proteins
'''Interleukins  '''
*** Regulation of the production of antiproliferative proteins
 
** '''Interleukins''' '''(ILs)'''
*  
*** Regulation of immune cell differentiation and activation  
 
*** May be pro- or anti-inflammatory  
'''Chemokines  '''
** '''Chemokines'''
 
*** Act as chemoattractants
*  
*** Recruitment of leukocytes
 
** '''Colony-stimulating factors'''  
'''Colony-stimulating factors  '''
*** Induction of hematopoietic progenitor cell proliferation and differentiation  
 
** '''Tumor necrosis factor (TNF)''' 
*  
*** Activation of T cells (cytotoxic)
 
'''Tumor necrosis factor'''  


*  
*  
Line 34: Line 33:


*In SARS coronavirus (SARS-CoV) and MERS coronavirus (MERS-CoV), cytokine storms have been associated with acute respiratory distress syndrome (ARDS). (2 in kuppali)
*In SARS coronavirus (SARS-CoV) and MERS coronavirus (MERS-CoV), cytokine storms have been associated with acute respiratory distress syndrome (ARDS). (2 in kuppali)
*The pathogenesis of SARS or MERS  infection may be related to a excessive or dysregulated cytokine release.
*In acute SARS-CoV and MERS-CoV infection, there is delayed release of cytokines and chemokines. (36) However, later during the infection there is rapid release of cytokines and chemokines which attract  neutrophils and monocytes. This excessive infiltration of neutrophils and monocytes in the lung causes lung damage.
*In the early stages of SARS-CoV and MERS-CoV infection, there is delayed release of cytokines and chemokines. (36) However, later during the infection there is rapid release of cytokines and chemokines which attract  neutrophils and monocytes. This excessive infiltration of neutrophils and monocytes in the lung causes lung damage.
*Proinflammatory cytokines that have a role in ARDS include:44–4  
*Proinflammatory cytokines that have a role in ARDS include:44–4
**IL-1β
**Proinflammatory cytokines (IL-6, IL-8, IL-1β, granulocytemacrophage colony-stimulating factor, and reactive oxygen species)  
**IL-6
**Proinflammatory chemokines (such as CCL2, CCL-5, IFNγ -induced protein10 (IP-10), and CCL3)  
**IL-8 (CXCL8)
**CCL-2 (MCP-1)
**CCL-3 (Macrophage inflammatory protein-1A)
**CCL-5
**IFNγ -induced protein10 (IP-10, CXCL10)
**Granulocytemacrophage colony-stimulating factor (GM-CSF)  


* IFN-I or IFN-α/β play an important role in antiviral immune defense. 35,36
* IFN-I or IFN-α/β play an important role in antiviral immune defense. 35,36
**The IFN-α/β receptors on the surface of accumulated macrophages receive activating signals, this results in more production of chemokines by these cells which in turn results in further accumulation of macrophages. Therefore, more proinflammatory cytokines are produced and therefore the infection becomes more severe.
**IFN-α/β or the proinflammatory cytokines produced by macrophages induce T-cell apoptosis, and this delays the antiviral immune defense process.
** Vascular leakage in the lungs and alveolar edema are caused by rapid cytokine increase that induce apoptosis in lung cells, which in turn results in hypoxia


* The IFN-α/β receptors on the surface of accumulated macrophages receive activating signals, this results in more production of chemokines by these cells which in turn results in further accumulation of macrophages. More proinflammatory cytokines are produced and therefore the infection becomes more severe.
* Cytokines change over time in patients with sepsis:<ref name="pmid22390970" />
 
** In the early stages of the infection (minutes to hours), cytokines  such as TNF and IL-1, and chemokines such as IL-8 and MCP-1 increase.
* IFN-α/β or proinflammatory cytokines  produced by macrophages induce T-cell apoptosis , which delays the antiviral defense process.
** Increase in IL-6 is followed.
* Rapid cytokine increase induces apoptosis in lung cells, which causes vascular leakage and alveolar edema, resulting in hypoxia .
** Later, IL-10 (anti-inflammatory cytokine) increases.  


=== COVID-19 and Cytokine Storm ===
=== COVID-19 and Cytokine Storm ===
Line 105: Line 112:




 
<s>Cytokine storm in the lung and systemic circulation causes acute lung injury (ALI) .(121) In the acute phase there is mononuclear and neutrophilic inflammatory response, followed by a chronic phase of fibroproliferation of collagen deposition in the lung tissue. (96)</s>


==<s>Overview</s>==
==<s>Overview</s>==

Revision as of 13:37, 11 July 2020

Associate Editor(s)-in-Chief: Shakiba Hassanzadeh, MD[1]

  • Cytokine storm is an immune reaction that is characterized by dysregulated and excessive release of proinflammatory cytokines.[1]
  • During sepsis, cytokine storm may be the cause of cell or organ injury.[2]

Cytokines

  • Cytokines are small proteins that are released for cell signaling.[1]
  • Cytokine types and their actions include:[1]
    • Interferons (INFs)
      • Key role in innate immunity
      • Regulation of the production of antiviral proteins
      • Regulation of the production of antiproliferative proteins
    • Interleukins (ILs)
      • Regulation of immune cell differentiation and activation  
      • May be pro- or anti-inflammatory  
    • Chemokines
      • Act as chemoattractants
      • Recruitment of leukocytes
    • Colony-stimulating factors  
      • Induction of hematopoietic progenitor cell proliferation and differentiation  
    • Tumor necrosis factor (TNF) 
      • Activation of T cells (cytotoxic)

Pathogenesis of ARDS by Cytokine Storm

  • In SARS coronavirus (SARS-CoV) and MERS coronavirus (MERS-CoV), cytokine storms have been associated with acute respiratory distress syndrome (ARDS). (2 in kuppali)
  • In acute SARS-CoV and MERS-CoV infection, there is delayed release of cytokines and chemokines. (36) However, later during the infection there is rapid release of cytokines and chemokines which attract neutrophils and monocytes. This excessive infiltration of neutrophils and monocytes in the lung causes lung damage.
  • Proinflammatory cytokines that have a role in ARDS include:44–4
    • IL-1β
    • IL-6
    • IL-8 (CXCL8)
    • CCL-2 (MCP-1)
    • CCL-3 (Macrophage inflammatory protein-1A)
    • CCL-5
    • IFNγ -induced protein10 (IP-10, CXCL10)
    • Granulocytemacrophage colony-stimulating factor (GM-CSF)
  • IFN-I or IFN-α/β play an important role in antiviral immune defense. 35,36
    • The IFN-α/β receptors on the surface of accumulated macrophages receive activating signals, this results in more production of chemokines by these cells which in turn results in further accumulation of macrophages. Therefore, more proinflammatory cytokines are produced and therefore the infection becomes more severe.
    • IFN-α/β or the proinflammatory cytokines produced by macrophages induce T-cell apoptosis, and this delays the antiviral immune defense process.
    • Vascular leakage in the lungs and alveolar edema are caused by rapid cytokine increase that induce apoptosis in lung cells, which in turn results in hypoxia
  • Cytokines change over time in patients with sepsis:[1]
    • In the early stages of the infection (minutes to hours), cytokines such as TNF and IL-1, and chemokines such as IL-8 and MCP-1 increase.
    • Increase in IL-6 is followed.
    • Later, IL-10 (anti-inflammatory cytokine) increases.

COVID-19 and Cytokine Storm

Proinflammatory Cytokines
  • Significant increase in pro-inflammatory cytokines (such as IL-6), reduction in CD+8 T cells, suppressed Th1 antiviral responses and increase in IL-10 (a Th2 cytokine) have been reported to be associated with severe COVID-19 infection. (kupalli) Therefore, it has been suggested that the pathogenesis of severe COVID-19 infection may be due to cytokine storm and suppressed Th1 antiviral responses. (kupalli)
  • High levels of expression of IL-1B, IFN-γ , IP-10, and monocyte hemoattractant protein 1 (MCP-1) have been detected in patientswith COVID-19.  
  • These inflammatory cytokines may activate the Thelper type 1 (Th1) cell response.47 Th1 activation is a key event in the activation of specific immunity.48
  • The serum levels of IL-2R and IL-6 in patients with COVID-19 are positively correlated with the severity of the disease (i.e., critically ill patients > severely ill patients > ordinary patients).49  
  • ther studies have found that, compared with COVID-19 patients from general wards, patients in the intensive care unit (ICU) display increased serum levels of granulocyte colony-stimulating factor, IP-10, MCP-1, macrophage inflammatory protein-1A, and TNF-α. The above studies suggest that the cytokine storm is positively correlated with disease severity.47
Anti-inflammatory Cytokines
  • In contrast to SARS infection, patients with COVID-19 infection have high levels of IL-4 and IL-10 (secreted by Th2 cells), which are antiinflammatory cytokines.
Cytokines Involved in COVID-19-Associated-Cytokine Storm
Proinflammatory Interferones
  • IFN-γ
Interleukines
  • IL-1β
  • IL-6
Chemokines
  • CCL-2 (MCP-1)
  • CCL-3 (Macrophage inflammatory protein-1A)
  • CCL-5
  • IL-8 (CXCL8)
  • IP-10 (CXCL10)
Colony-stimulating

factors  

  • GM-CSF
Tumor necrosis

factor  

  • TNF-α
Anti-inflammatory Interleukines
  • IL-4
  • IL-10



Cytokine storm in the lung and systemic circulation causes acute lung injury (ALI) .(121) In the acute phase there is mononuclear and neutrophilic inflammatory response, followed by a chronic phase of fibroproliferation of collagen deposition in the lung tissue. (96)

Overview

COVID-19-Associated Hematologic Findings

Pathophysiology and Causes

Epidemiology

  • Leukocytosis is seen in 11.4% of patients with severe COVID-19 infection compared to 4.8% of patients with non-severe infection.[5][6]
  • Increase in CRP is seen in 81.5% of patients with severe COVID-19 infection compared to 56.4% of patients with non-severe infection.[5][6]
  • Increase in procalcitonin is seen in 13.7% of patients with severe COVID-19 infection compared to 3.7% of patients with non-severe infection.[5][6]
  • Increase in AST is seen in 39.4% of patients with severe COVID-19 infection compared to 18.2% of patients with non-severe infection.[5][6]
  • Increase in ALT is seen in 28.1% of patients with severe COVID-19 infection compared to 19.8% of patients with non-severe infection.[5][6]
  • Increase in LDH is seen in 58.1% of patients with severe COVID-19 infection compared to 37.2% of patients with non-severe infection.[5][6]
  • MDW was found to be increased in all patients with COVID-19 infection, particularly in those with the worst conditions.[6]
  • Increase in total bilirubin is seen in 13.3% of patients with severe COVID-19 infection compared to 9.9% of patients with non-severe infection.[5][6]
  • Increase in creatinine is seen in 4.3% of patients with severe COVID-19 infection compared to 1% of patients with non-severe infection.[5][6]
  • Thrombocytosis has been reported in 4% of patients with COVID-19 infection.[7]

Clinical Significance

Laboratory findings in COVID-19 infection may indicate clinical abnormalities, including:

  • In patients with COVID-19 infection, leukocytosis may be an indication of a bacterial infection or superinfection.[6]
  • In patients with COVID-19 infection, increase in CRP may be an indication of severe viral infection or sepsis and viremia.[6]
  • In patients with COVID-19 infection, increase in procalcitonin may be an indication of bacterial infection or superinfection.[6]
  • There have been different reports regarding the association of increase in ferritin with death in COVID-19 infection; for example, there has been a report that increase in ferritin is associated with acute respiratory distress syndrome (ARDS) but not death[8], while another one reports an association between increase in ferritin and death in COVID-19 infection[9]
  • In patients with COVID-19 infection, increase in aminotransferases may indicate injury to the liver or multi-system damage.[6]
  • In patients with COVID-19 infection, increase in aminotransferases may indicate injury to the liver or multi-system damage.[6]
  • In patients with COVID-19 infection, increase in LDH may indicate injury to the lungs or multi-system damage.[6]
  • In patients with COVID-19 infection, increase in total bilirubin may indicate injury to the liver.[6]
  • In patients with COVID-19 infection, increase in creatinine may indicate injury to the kidneys.[6]
  • In patients with COVID-19 infection, increase in cardiac troponins may indicate cardiac injury.[6]
  • In patients with COVID-19 infection, decrease in albumin may indicate liver function abnormality.[6]
  • Increase in IL-6 has been reported to be associated with death in COVID-19 infection.[8]


References

  1. ↑ 1.0 1.1 1.2 1.3 Tisoncik JR, Korth MJ, Simmons CP, Farrar J, Martin TR, Katze MG (2012). "Into the eye of the cytokine storm". Microbiol Mol Biol Rev. 76 (1): 16–32. doi:10.1128/MMBR.05015-11. PMC 3294426. PMID 22390970.
  2. ↑ Chousterman BG, Swirski FK, Weber GF (2017). "Cytokine storm and sepsis disease pathogenesis". Semin Immunopathol. 39 (5): 517–528. doi:10.1007/s00281-017-0639-8. PMID 28555385.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 Frater JL, Zini G, d'Onofrio G, Rogers HJ (2020). "COVID-19 and the clinical hematology laboratory". Int J Lab Hematol. 42 Suppl 1: 11–18. doi:10.1111/ijlh.13229. PMC 7264622 Check |pmc= value (help). PMID 32311826 Check |pmid= value (help).
  4. ↑ Meisner M (2014). "Update on procalcitonin measurements". Ann Lab Med. 34 (4): 263–73. doi:10.3343/alm.2014.34.4.263. PMC 4071182. PMID 24982830.
  5. ↑ 5.0 5.1 5.2 5.3 5.4 5.5 5.6 5.7
  6. ↑ 6.00 6.01 6.02 6.03 6.04 6.05 6.06 6.07 6.08 6.09 6.10 6.11 6.12 6.13 6.14 6.15 6.16 6.17 6.18 Lippi G, Plebani M (2020). "The critical role of laboratory medicine during coronavirus disease 2019 (COVID-19) and other viral outbreaks". Clin Chem Lab Med. 58 (7): 1063–1069. doi:10.1515/cclm-2020-0240. PMID 32191623 Check |pmid= value (help).
  7. ↑ Chen N, Zhou M, Dong X, Qu J, Gong F, Han Y; et al. (2020). "Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study". Lancet. 395 (10223): 507–513. doi:10.1016/S0140-6736(20)30211-7. PMC 7135076 Check |pmc= value (help). PMID 32007143 Check |pmid= value (help).
  8. ↑ 8.0 8.1 Wu C, Chen X, Cai Y, Xia J, Zhou X, Xu S; et al. (2020). "Risk Factors Associated With Acute Respiratory Distress Syndrome and Death in Patients With Coronavirus Disease 2019 Pneumonia in Wuhan, China". JAMA Intern Med. doi:10.1001/jamainternmed.2020.0994. PMC 7070509 Check |pmc= value (help). PMID 32167524 Check |pmid= value (help).
  9. ↑ Zhou F, Yu T, Du R, Fan G, Liu Y, Liu Z; et al. (2020). "Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study". Lancet. 395 (10229): 1054–1062. doi:10.1016/S0140-6736(20)30566-3. PMC 7270627 Check |pmc= value (help). PMID 32171076 Check |pmid= value (help).


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