دورية أكاديمية
Cachexia causes time-dependent activation of the inflammasome in the liver.
| العنوان: | Cachexia causes time-dependent activation of the inflammasome in the liver. |
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| المؤلفون: | das Neves RX; Cancer Metabolism Research Group, Department of Surgery and LIM26-HCFMUSP Faculdade de Medicina, University of São Paulo, São Paulo, Brazil.; LICI, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA., Yamashita AS; Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil., Riccardi DMR; Cancer Metabolism Research Group, Department of Surgery and LIM26-HCFMUSP Faculdade de Medicina, University of São Paulo, São Paulo, Brazil., Köhn-Gaone J; Department of Surgery, School of Veterinary Medicine and Animal Science of University of São Paulo-FMVZ/USP, São Paulo, Brazil., Camargo RG; Cancer Metabolism Research Group, Department of Surgery and LIM26-HCFMUSP Faculdade de Medicina, University of São Paulo, São Paulo, Brazil., Neto NI; Department of Physiology, Federal University of São Paulo, São Paulo, Brazil., Caetano D; Cancer Metabolism Research Group, Department of Surgery and LIM26-HCFMUSP Faculdade de Medicina, University of São Paulo, São Paulo, Brazil., Gomes SP; Cancer Metabolism Research Group, Department of Surgery and LIM26-HCFMUSP Faculdade de Medicina, University of São Paulo, São Paulo, Brazil.; Department of Surgery, School of Veterinary Medicine and Animal Science of University of São Paulo-FMVZ/USP, São Paulo, Brazil., Santos FH; Laboratory of Adipose Tissue Biology, Center for Integrated Biotechnology, University of Mogi das Cruzes, São Paulo, Brazil., Lima JDCC; Cancer Metabolism Research Group, Department of Surgery and LIM26-HCFMUSP Faculdade de Medicina, University of São Paulo, São Paulo, Brazil., Batista ML Jr; Laboratory of Adipose Tissue Biology, Center for Integrated Biotechnology, University of Mogi das Cruzes, São Paulo, Brazil., Rosa-Neto JC; Immunometabolism Research Group, Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil., Martins De Alcântara PS; Cancer Metabolism Research Group, Department of Surgery and LIM26-HCFMUSP Faculdade de Medicina, University of São Paulo, São Paulo, Brazil., Maximiano LF; Cancer Metabolism Research Group, Department of Surgery and LIM26-HCFMUSP Faculdade de Medicina, University of São Paulo, São Paulo, Brazil., Otoch JP; LICI, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA., Trinchieri G; LICI, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA., Tirnitz-Parker JEE; Liver Disease and Regeneration Laboratory, School of Pharmacy and Biomedical Sciences and Curtin Health Innovation Research Institute, Curtin University, Bentley, Western Australia, Australia., Seelaender M; Cancer Metabolism Research Group, Department of Surgery and LIM26-HCFMUSP Faculdade de Medicina, University of São Paulo, São Paulo, Brazil. |
| المصدر: | Journal of cachexia, sarcopenia and muscle [J Cachexia Sarcopenia Muscle] 2023 Aug; Vol. 14 (4), pp. 1621-1630. Date of Electronic Publication: 2023 May 12. |
| نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: John Wiley & Sons Ltd on behalf of Society on Sarcopenia, Cachexia and Wasting Disorders Country of Publication: Germany NLM ID: 101552883 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2190-6009 (Electronic) Linking ISSN: 21905991 NLM ISO Abbreviation: J Cachexia Sarcopenia Muscle Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: 2015- : Berlin : John Wiley & Sons Ltd on behalf of Society on Sarcopenia, Cachexia and Wasting Disorders Original Publication: Heidelburg : Springer-Verlag |
| مواضيع طبية MeSH: | Colonic Neoplasms*/complications , Carcinosarcoma*/complications , Carcinosarcoma*/metabolism, Humans ; Male ; Rats ; Animals ; Cachexia/pathology ; Inflammasomes/metabolism ; Liver/metabolism ; Inflammation/metabolism |
| مستخلص: | Background: Cachexia is a wasting syndrome associated with systemic inflammation and metabolic disruption. Detection of the early signs of the disease may contribute to the effective attenuation of associated symptoms. Despite playing a central role in the control of metabolism and inflammation, the liver has received little attention in cachexia. We previously described relevant disruption of metabolic pathways in the organ in an animal model of cachexia, and herein, we adopt the same model to investigate temporal onset of inflammation in the liver. The aim was thus to study inflammation in rodent liver in the well-characterized cachexia model of Walker 256 carcinosarcoma and, in addition, to describe inflammatory alterations in the liver of one cachectic colon cancer patient, as compared to one control and one weight-stable cancer patient. Methods: Colon cancer patients (one weight stable [WSC] and one cachectic [CC]) and one patient undergoing surgery for cholelithiasis (control, n = 1) were enrolled in the study, after obtainment of fully informed consent. Eight-week-old male rats were subcutaneously inoculated with a Walker 256 carcinosarcoma cell suspension (2 × 10 7 cells in 1.0 mL; tumour-bearing [T]; or phosphate-buffered saline-controls [C]). The liver was excised on Days 0 (n = 5), 7 (n = 5) and 14 (n = 5) after tumour cell injection. Results: In rodent cachexia, we found progressively higher numbers of CD68 + myeloid cells in the liver along cancer-cachexia development. Similar findings are described for CC, whose liver showed infiltration of the same cell type, compared with both WSC and control patient organs. In advanced rodent cachexia, hepatic phosphorylated c-Jun N-terminal kinase protein content and the inflammasome pathway protein expression were increased in relation to baseline (P < 0.05). These changes were accompanied by augmented expression of the active interleukin-1β (IL-1β) form (P < 0.05 for both circulating and hepatic content). Conclusions: The results show that cancer cachexia is associated with an increase in the number of myeloid cells in rodent and human liver and with modulation of hepatic inflammasome pathway. The latter contributes to the aggravation of systemic inflammation, through increased release of IL-1β. (© 2023 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of Society on Sarcopenia, Cachexia and Wasting Disorders.) |
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| فهرسة مساهمة: | Keywords: cancer cachexia; inflammasome; inflammation; liver; myeloid cells |
| المشرفين على المادة: | 0 (Inflammasomes) |
| تواريخ الأحداث: | Date Created: 20230513 Date Completed: 20230807 Latest Revision: 20230807 |
| رمز التحديث: | 20230808 |
| مُعرف محوري في PubMed: | PMC10401524 |
| DOI: | 10.1002/jcsm.13236 |
| PMID: | 37177862 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 2190-6009 |
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| DOI: | 10.1002/jcsm.13236 |