Complement C4a: Difference between revisions

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'''Complement C4a''' is a glycoprotein and peptide that is expressed, primarily in the liver and in [[macrophage]]s, in response to acute [[inflammation]] or tissue injury.<ref name="MeshB">https://meshb.nlm.nih.gov/record/ui?name=Complement%20C4</ref><ref name="Behairy2013">[https://www.wjgnet.com/1948-5182/full/v5/i8/445.htm Serum complement C4a and its relation to liver fibrosis in children with chronic hepatitis C]</ref> Complement C3 also has a role in [[allergy]] response.<ref name="PMC2725201">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2725201</ref>
'''Complement C4a''' or '''complement component 4a''' is a [[glycoprotein]] and peptide that is expressed, primarily in the liver and in [[macrophage]]s, in response to acute [[inflammation]] or tissue injury.<ref name="MeshB">{{Cite web | url = https://meshb.nlm.nih.gov/record/ui?name=Complement%20C4a | title = Complement C4a MeSH Descriptor Data 2022 {{!}} MeSH Browser | last = | first = | authorlink = | date = | website = [[National Institutes of Health]]| archive-url = | archive-date = |url-status = | access-date=2022-01-24}}</ref><ref name="Behairy2013">{{Cite journal | title = Serum complement C4a and its relation to liver fibrosis in children with chronic hepatitis C | date = 2013-08-27 | url = https://www.wjgnet.com/1948-5182/full/v5/i8/445.htm|journal=World Journal of Hepatology|volume=5 | issue = 8 | pages = 445–451 | last = Behairy|first = Behairy E. | last2 = El-Mashad | first2 = Ghada M. | last3 = Abd-Elghany | first3 = Ragab S. | last4 = Ghoneim | first4 = Enas M. | last5 = Sira | first5 = Mostafa M.|language=en|doi=10.4254/wjh.v5.i8.445}}</ref> Complement C4a is part of the Complement C4 family.<ref name="PMC2725201">{{Cite journal | title = The Role of the Anaphylatoxins in Health and Disease | date = Sep 2009 | url = https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2725201/|journal=Molecular immunology|volume=46 | issue = 14 | pages = 2753–2766 | last = Klos | first = Andreas | authorlink = | last2 = Tenner | first2 = Andrea J. | authorlink2 = | last3 = Johswich | first3 = Kay-Ole | author-link3 = | last4 = Ager | first4 = Rahasson R. | author-link4 = | last5 = Reis | first5 = Edimara S. | author-link5 = | last6 = Köhl | first6 = Jörg | author-link6 = |doi=10.1016/j.molimm.2009.04.027|pmc=2725201|pmid=19477527|access-date=|issn=0161-5890|quote=|via=}}</ref>


==ME/CFS==
==ME/CFS==
Increased C4a levels have been found one to six hours after exercise challenge tests in [[ME/CFS]] patients but not in healthy controls.<ref name ="Sorensen2003">[https://www.ncbi.nlm.nih.gov/pubmed/12897748 Sorensen B, Streib JE, Strand M, Make B, Giclas PC, Fleshner M, Jones JF. Complement activation in a model of chronic fatigue syndrome.J Allergy Clin Immunol. 2003 Aug;112(2):397-403. pmid 12897748]</ref>  
Increased C4a levels have been found one to six hours after exercise challenge tests in [[ME/CFS]] patients but not in healthy controls.<ref name="Sorensen2003"/>


{{Quote frame|quote=A significant correlation was found [in Chronic Fatigue Syndrome patients] between the increase in C4a and total symptom score (P < .05) and the fol- lowing individual symptoms: headaches (P < .02), joint problems (P < .05), and thinking difficulty (P < .03), through the use of 1-sided tests.<ref name="Sorensen2003"/>|source=Sorensen et al, 2003}}
{{Quote frame|quote=A significant correlation was found [in Chronic Fatigue Syndrome patients] between the increase in C4a and total symptom score (P < .05) and the following individual symptoms: headaches (P < .02), joint problems (P < .05), and thinking difficulty (P < .03), through the use of 1-sided tests.<ref name="Sorensen2003"/>|source=Sorensen et al, 2003}}


Nijs et al. (2010) found a strong relation between the change in [[complement C4a]] level and an increase in post-exertional pain and fatigue in ME/CFS patients.<ref name="Nijs2010">{{Cite journal|last=Nijs|first=J.|author-link=Jo Nijs|last2=Van Oosterwijck|first2=J.|author-link2=Jessica Van Oosterwijck|last3=Meeus|first3=M.|author-link3=Mira Meeus|last4=Lambrecht|first4=L.|author-link4=|last5=Metzger|first5=K.|author-link5=|last6=Frémont|first6=M.|last7=Paul|first7=L.|date=2010|title=Unravelling the nature of postexertional malaise in myalgic encephalomyelitis/chronic fatigue syndrome: the role of elastase, complement C4a and interleukin-1β|url=https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2796.2009.02178.x|journal=Journal of Internal Medicine|language=en|volume=267|issue=4|pages=418–435|doi=10.1111/j.1365-2796.2009.02178.x|issn=1365-2796|quote=|via=}}</ref> Previously, complement C4a, in combination with other proteins, was being considered as a potential [[biomarker|marker]] of [[post-exertional malaise]] in [[ME/CFS]].<ref name="Sorensen2009"/>
Nijs et al. (2010) found a strong relation between the change in [[complement C4a]] level and an increase in post-exertional [[pain]] and [[fatigue]] in ME/CFS patients.<ref name="Nijs2010">{{Cite journal | last = Nijs | first = J. | authorlink = Jo Nijs | last2 = Van Oosterwijck | first2 = J. | authorlink2 = Jessica Van Oosterwijck | last3 = Meeus | first3 = M. | author-link3 = Mira Meeus | last4 = Lambrecht | first4 = L. | author-link4 = | last5 = Metzger | first5 = K. | author-link5 = | last6 = Frémont | first6 = M. | last7 = Paul | first7 = L. | date = 2010 | title=Unravelling the nature of postexertional malaise in myalgic encephalomyelitis/chronic fatigue syndrome: the role of elastase, complement C4a and interleukin-1β | url = https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2796.2009.02178.x|journal=Journal of Internal Medicine|language=en|volume=267 | issue = 4 | pages = 418–435|doi=10.1111/j.1365-2796.2009.02178.x|issn=1365-2796|quote=|via=}}</ref> Previously, complement C4a, in combination with other proteins, was being considered as a potential diagnostic [[biomarker]] of [[post-exertional malaise]] in [[ME/CFS]].<ref name="Sorensen2009" />


==Notable studies ==
==Notable studies ==
*2009, Transcriptional Control of Complement Activation in an Exercise Model of Chronic Fatigue Syndrome<ref name="Sorensen2009">{{Cite journal|last=Sorensen|first=Bristol|author-link=|last2=Jones|first2=James F|author-link2=|last3=Vernon|first3=Suzanne D|author-link3=Suzanne Vernon|last4=Rajeevan|first4=Mangalathu S|author-link4=Mangalathu Rajeevan|date=Jan 2009|title=Transcriptional Control of Complement Activation in an Exercise Model of Chronic Fatigue Syndrome|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2583111/|journal=Molecular Medicine|volume=15|issue=1-2|pages=34–42|doi=10.2119/molmed.2008.00098|pmc=PMC2583111|pmid=19015737|quote=|via=}}</ref> [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2583111/pdf/mol-15-34.pdf (Full text)]  
*2003, Complement activation in a model of chronic fatigue syndrome<ref name="Sorensen2003">{{Cite journal | title = Complement activation in a model of chronic fatigue syndrome | date = Aug 2003 | url = https://pubmed.ncbi.nlm.nih.gov/12897748/|journal=The Journal of Allergy and Clinical Immunology|volume=112 | issue = 2 | pages = 397–403 | last = Sorensen | first = Bristol | authorlink = | last2 = Streib | first2 = Joanne E. | authorlink2 = | last3 = Strand | first3 = Matthew | author-link3 = | last4 = Make | first4 = Barry | author-link4 = | last5 = Giclas | first5 = Patricia C. | author-link5 = | last6 = Fleshner | first6 = Monika | author-link6 = | last7 = Jones | first7 = James F.|doi=10.1067/mai.2003.1615|pmc=|pmid=12897748|access-date=|issn=0091-6749|quote=|via=}}</ref> - [https://pubmed.ncbi.nlm.nih.gov/12897748/ (Abstract)]
*2009, Transcriptional Control of Complement Activation in an Exercise Model of Chronic Fatigue Syndrome<ref name="Sorensen2009">{{Cite journal | last = Sorensen | first = Bristol | authorlink = | last2 = Jones | first2 = James F | authorlink2 = | last3 = Vernon | first3 = Suzanne D | author-link3 = Suzanne Vernon | last4 = Rajeevan | first4 = Mangalathu S | author-link4 = Mangalathu Rajeevan | date = Jan 2009 | title = Transcriptional Control of Complement Activation in an Exercise Model of Chronic Fatigue Syndrome | url =https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2583111/|journal=Molecular Medicine|volume=15 | issue = 1-2 | pages = 34–42|doi=10.2119/molmed.2008.00098|pmc=PMC2583111|pmid=19015737|quote=|via=}}</ref> - [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2583111/pdf/mol-15-34.pdf (Full text)]
*2010, Unravelling the nature of postexertional malaise in myalgic encephalomyelitis/chronic fatigue syndrome: the role of elastase, complement C4a and interleukin-1β<ref name="Nijs2010"/> - [https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2796.2009.02178.x (Abstract)]


==See also ==
==See also ==
*[[Exercise]]
*[[Exercise]]
*[[Post-exertional malaise]]
*[[Post-exertional malaise]]
*[[Anaphylaxis]]
*[[Cognitive dysfunction]] including thinking problems
*[[Headache]]s


==Learn more ==
==Learn more ==

Latest revision as of 17:06, April 3, 2023

Complement C4a or complement component 4a is a glycoprotein and peptide that is expressed, primarily in the liver and in macrophages, in response to acute inflammation or tissue injury.[1][2] Complement C4a is part of the Complement C4 family.[3]

ME/CFS[edit | edit source]

Increased C4a levels have been found one to six hours after exercise challenge tests in ME/CFS patients but not in healthy controls.[4]

A significant correlation was found [in Chronic Fatigue Syndrome patients] between the increase in C4a and total symptom score (P < .05) and the following individual symptoms: headaches (P < .02), joint problems (P < .05), and thinking difficulty (P < .03), through the use of 1-sided tests.[4] — Sorensen et al, 2003

Nijs et al. (2010) found a strong relation between the change in complement C4a level and an increase in post-exertional pain and fatigue in ME/CFS patients.[5] Previously, complement C4a, in combination with other proteins, was being considered as a potential diagnostic biomarker of post-exertional malaise in ME/CFS.[6]

Notable studies[edit | edit source]

  • 2003, Complement activation in a model of chronic fatigue syndrome[4] - (Abstract)
  • 2009, Transcriptional Control of Complement Activation in an Exercise Model of Chronic Fatigue Syndrome[6] - (Full text)
  • 2010, Unravelling the nature of postexertional malaise in myalgic encephalomyelitis/chronic fatigue syndrome: the role of elastase, complement C4a and interleukin-1β[5] - (Abstract)

See also[edit | edit source]

Learn more[edit | edit source]

References[edit | edit source]

  1. "Complement C4a MeSH Descriptor Data 2022 | MeSH Browser". National Institutes of Health. Retrieved January 24, 2022.
  2. Behairy, Behairy E.; El-Mashad, Ghada M.; Abd-Elghany, Ragab S.; Ghoneim, Enas M.; Sira, Mostafa M. (August 27, 2013). "Serum complement C4a and its relation to liver fibrosis in children with chronic hepatitis C". World Journal of Hepatology. 5 (8): 445–451. doi:10.4254/wjh.v5.i8.445.
  3. Klos, Andreas; Tenner, Andrea J.; Johswich, Kay-Ole; Ager, Rahasson R.; Reis, Edimara S.; Köhl, Jörg (September 2009). "The Role of the Anaphylatoxins in Health and Disease". Molecular immunology. 46 (14): 2753–2766. doi:10.1016/j.molimm.2009.04.027. ISSN 0161-5890. PMC 2725201. PMID 19477527.
  4. 4.0 4.1 4.2 Sorensen, Bristol; Streib, Joanne E.; Strand, Matthew; Make, Barry; Giclas, Patricia C.; Fleshner, Monika; Jones, James F. (August 2003). "Complement activation in a model of chronic fatigue syndrome". The Journal of Allergy and Clinical Immunology. 112 (2): 397–403. doi:10.1067/mai.2003.1615. ISSN 0091-6749. PMID 12897748.
  5. 5.0 5.1 Nijs, J.; Van Oosterwijck, J.; Meeus, M.; Lambrecht, L.; Metzger, K.; Frémont, M.; Paul, L. (2010). "Unravelling the nature of postexertional malaise in myalgic encephalomyelitis/chronic fatigue syndrome: the role of elastase, complement C4a and interleukin-1β". Journal of Internal Medicine. 267 (4): 418–435. doi:10.1111/j.1365-2796.2009.02178.x. ISSN 1365-2796.
  6. 6.0 6.1 Sorensen, Bristol; Jones, James F; Vernon, Suzanne D; Rajeevan, Mangalathu S (January 2009). "Transcriptional Control of Complement Activation in an Exercise Model of Chronic Fatigue Syndrome". Molecular Medicine. 15 (1–2): 34–42. doi:10.2119/molmed.2008.00098. PMC 2583111. PMID 19015737.