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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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) |
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cancer cachexia complement system activation inflammation Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 |
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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 |
_version_ |
1718412774126649344 |