Activation of the Complement System in Patients with Cancer Cachexia

Systemic inflammation is thought to underlie many of the metabolic manifestations of cachexia in cancer patients. The complement system is an important component of innate immunity that has been shown to contribute to metabolic inflammation. We hypothesized that systemic inflammation in patients wit...

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Autores principales: Min Deng, Rianne D. W. Vaes, Annemarie A. J. H. M. van Bijnen, Steven W. M. Olde Damink, Sander S. Rensen
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Publicado: MDPI AG 2021
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spelling oai:doaj.org-article:50e88f3df25541a1969440aef39fbfde2021-11-25T17:03:46ZActivation of the Complement System in Patients with Cancer Cachexia10.3390/cancers132257672072-6694https://doaj.org/article/50e88f3df25541a1969440aef39fbfde2021-11-01T00:00:00Zhttps://www.mdpi.com/2072-6694/13/22/5767https://doaj.org/toc/2072-6694Systemic inflammation is thought to underlie many of the metabolic manifestations of cachexia in cancer patients. The complement system is an important component of innate immunity that has been shown to contribute to metabolic inflammation. We hypothesized that systemic inflammation in patients with cancer cachexia was associated with complement activation. Systemic C3a levels were higher in cachectic patients with inflammation (<i>n</i> = 23, C-reactive protein (CRP) ≥ 10 mg/L) as compared to patients without inflammation (<i>n</i> = 26, CRP < 10 mg/L) or without cachexia (<i>n</i> = 13) (medians 102.4 (IQR 89.4–158.0) vs. 81.4 (IQR 47.9–124.0) vs. 61.6 (IQR 46.8–86.8) ng/mL, respectively, <i>p</i> = 0.0186). Accordingly, terminal complement complex (TCC) concentrations gradually increased in these patient groups (medians 2298 (IQR 2022–3058) vs. 1939 (IQR 1725–2311) vs. 1805 (IQR 1552–2569) mAU/mL, respectively, <i>p</i> = 0.0511). C3a and TCC concentrations were strongly correlated (r<sub>s</sub> = 0.468, <i>p</i> = 0.0005). Although concentrations of C1q and mannose-binding lectin did not differ between groups, C1q levels were correlated with both C3a and TCC concentrations (r<sub>s</sub> = 0.394, <i>p</i> = 0.0042 and r<sub>s</sub> = 0.300, <i>p</i> = 0.0188, respectively). In conclusion, systemic inflammation in patients with cancer cachexia is associated with the activation of key effector complement factors. The correlations between C1q and C3a/TCC suggest that the classical complement pathway could play a role in complement activation in patients with pancreatic cancer.Min DengRianne D. W. VaesAnnemarie A. J. H. M. van BijnenSteven W. M. Olde DaminkSander S. RensenMDPI AGarticlecancer cachexiacomplement system activationinflammationNeoplasms. Tumors. Oncology. Including cancer and carcinogensRC254-282ENCancers, Vol 13, Iss 5767, p 5767 (2021)
institution DOAJ
collection DOAJ
language EN
topic cancer cachexia
complement system activation
inflammation
Neoplasms. Tumors. Oncology. Including cancer and carcinogens
RC254-282
spellingShingle cancer cachexia
complement system activation
inflammation
Neoplasms. Tumors. Oncology. Including cancer and carcinogens
RC254-282
Min Deng
Rianne D. W. Vaes
Annemarie A. J. H. M. van Bijnen
Steven W. M. Olde Damink
Sander S. Rensen
Activation of the Complement System in Patients with Cancer Cachexia
description Systemic inflammation is thought to underlie many of the metabolic manifestations of cachexia in cancer patients. The complement system is an important component of innate immunity that has been shown to contribute to metabolic inflammation. We hypothesized that systemic inflammation in patients with cancer cachexia was associated with complement activation. Systemic C3a levels were higher in cachectic patients with inflammation (<i>n</i> = 23, C-reactive protein (CRP) ≥ 10 mg/L) as compared to patients without inflammation (<i>n</i> = 26, CRP < 10 mg/L) or without cachexia (<i>n</i> = 13) (medians 102.4 (IQR 89.4–158.0) vs. 81.4 (IQR 47.9–124.0) vs. 61.6 (IQR 46.8–86.8) ng/mL, respectively, <i>p</i> = 0.0186). Accordingly, terminal complement complex (TCC) concentrations gradually increased in these patient groups (medians 2298 (IQR 2022–3058) vs. 1939 (IQR 1725–2311) vs. 1805 (IQR 1552–2569) mAU/mL, respectively, <i>p</i> = 0.0511). C3a and TCC concentrations were strongly correlated (r<sub>s</sub> = 0.468, <i>p</i> = 0.0005). Although concentrations of C1q and mannose-binding lectin did not differ between groups, C1q levels were correlated with both C3a and TCC concentrations (r<sub>s</sub> = 0.394, <i>p</i> = 0.0042 and r<sub>s</sub> = 0.300, <i>p</i> = 0.0188, respectively). In conclusion, systemic inflammation in patients with cancer cachexia is associated with the activation of key effector complement factors. The correlations between C1q and C3a/TCC suggest that the classical complement pathway could play a role in complement activation in patients with pancreatic cancer.
format article
author Min Deng
Rianne D. W. Vaes
Annemarie A. J. H. M. van Bijnen
Steven W. M. Olde Damink
Sander S. Rensen
author_facet Min Deng
Rianne D. W. Vaes
Annemarie A. J. H. M. van Bijnen
Steven W. M. Olde Damink
Sander S. Rensen
author_sort Min Deng
title Activation of the Complement System in Patients with Cancer Cachexia
title_short Activation of the Complement System in Patients with Cancer Cachexia
title_full Activation of the Complement System in Patients with Cancer Cachexia
title_fullStr Activation of the Complement System in Patients with Cancer Cachexia
title_full_unstemmed Activation of the Complement System in Patients with Cancer Cachexia
title_sort activation of the complement system in patients with cancer cachexia
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/50e88f3df25541a1969440aef39fbfde
work_keys_str_mv AT mindeng activationofthecomplementsysteminpatientswithcancercachexia
AT riannedwvaes activationofthecomplementsysteminpatientswithcancercachexia
AT annemarieajhmvanbijnen activationofthecomplementsysteminpatientswithcancercachexia
AT stevenwmoldedamink activationofthecomplementsysteminpatientswithcancercachexia
AT sandersrensen activationofthecomplementsysteminpatientswithcancercachexia
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