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Cancer cachexia induces morphological and inflammatory changes in the intestinal mucosa

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  • معلومة اضافية
    • بيانات النشر:
      Wiley, 2019.
    • الموضوع:
      2019
    • Collection:
      LCC:Diseases of the musculoskeletal system
      LCC:Human anatomy
    • نبذة مختصرة :
      Abstract Background Cachexia is a multifactorial and multiorgan syndrome associated with cancer and other chronic diseases and characterized by severe involuntary body weight loss, disrupted metabolism, inflammation, anorexia, fatigue, and diminished quality of life. This syndrome affects around 50% of patients with colon cancer and is directly responsible for the death of at least 20% of all cancer patients. Systemic inflammation has been recently proposed to underline most of cachexia‐related symptoms. Nevertheless, the exact mechanisms leading to the initiation of systemic inflammation have not yet been unveiled, as patients bearing the same tumour and disease stage may or may not present cachexia. We hypothesize a role for gut barrier disruption, which may elicit persistent immune activation in the host. To address this hypothesis, we analysed the healthy colon tissue, adjacent to the tumour. Methods Blood and rectosigmoid colon samples (20 cm distal to tumour margin) obtained during surgery, from cachectic (CC = 25) or weight stable (WSC = 20) colon cancer patients, who signed the informed consent form, were submitted to morphological (light microscopy), immunological (immunohistochemistry and flow cytometry), and molecular (quantification of inflammatory factors by Luminex® xMAP) analyses. Results There was no statistical difference in gender and age between groups. The content of plasma interleukin 6 (IL‐6) and IL‐8 was augmented in cachectic patients relative to those with stable weight (P = 0.047 and P = 0.009, respectively). The number of lymphocytic aggregates/field in the gut mucosa was higher in CC than in WSC (P = 0.019), in addition to those of the lamina propria (LP) eosinophils (P
    • File Description:
      electronic resource
    • ISSN:
      2190-6009
      2190-5991
    • Relation:
      https://doaj.org/toc/2190-5991; https://doaj.org/toc/2190-6009
    • الرقم المعرف:
      10.1002/jcsm.12449
    • الرقم المعرف:
      edsdoj.40a80ee10b8e4b038cbf44fc55727bd5