Regulation and function of IL‐22 in peritoneal adhesion formation after abdominal surgery
Qingbo Wang Yongming Huang Rui Zhou Ke Wu Wei Li Liang Shi Zefeng Xia Kaixiong Tao Guobin Wang Geng Wang
First published: 30 May 2019 https://doi.org/10.1111/wrr.12740
This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1111/wrr.12740.
ePDFPDFTOOLS SHARE
Abstract
Peritoneal adhesion occurs frequently after gastrointestinal/gynaecological surgery. Tissue repair and regeneration are very important during this process. IL‐22 is an important cytokine that is secreted from immune cells but functions on mesenchymal cells, such as mesothelial cells. The objective of this study was to investigate the roles of IL‐22 and its regulators during adhesion formation. Postsurgical peritoneal drainage fluid from patients and rodent models was examined by enzyme‐linked immunosorbent assay (ELISA) and fluorescence‐activated cell sorting (FACS). It was observed that IL‐22 expression in the abdominal cavity was rapidly induced 12 hours after surgery and then slowly decreased to a lower, steady level for up to 7 days after surgery. However, neutralizing IL‐22 at the time point at which the highest level of expression was observed failed to reduce adhesion, but neutralizing IL‐22 at a later time point, i.e., 3 days after surgery, prevented adhesion significantly. The IL‐22 receptor was induced on the mesothelial membrane, and IL‐22BP, an inhibitor of IL‐22, was reduced 3 days after surgery. Furthermore, IFN‐γ was identified to have the ability to induce IL‐22R, and IL‐18, which was induced by the infiltrating macrophages, was found to inhibit IL‐22BP expression both in vivo and in vitro. Together, these data suggest that IL‐22 may promote adhesion formation and that the regulation of IL‐22, IL‐22R, and IL‐22BP may have therapeutic potential to prevent adhesion formation after surgery without disturbing the normal immune process.
Qingbo Wang Yongming Huang Rui Zhou Ke Wu Wei Li Liang Shi Zefeng Xia Kaixiong Tao Guobin Wang Geng Wang
First published: 30 May 2019 https://doi.org/10.1111/wrr.12740
This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1111/wrr.12740.
ePDFPDFTOOLS SHARE
Abstract
Peritoneal adhesion occurs frequently after gastrointestinal/gynaecological surgery. Tissue repair and regeneration are very important during this process. IL‐22 is an important cytokine that is secreted from immune cells but functions on mesenchymal cells, such as mesothelial cells. The objective of this study was to investigate the roles of IL‐22 and its regulators during adhesion formation. Postsurgical peritoneal drainage fluid from patients and rodent models was examined by enzyme‐linked immunosorbent assay (ELISA) and fluorescence‐activated cell sorting (FACS). It was observed that IL‐22 expression in the abdominal cavity was rapidly induced 12 hours after surgery and then slowly decreased to a lower, steady level for up to 7 days after surgery. However, neutralizing IL‐22 at the time point at which the highest level of expression was observed failed to reduce adhesion, but neutralizing IL‐22 at a later time point, i.e., 3 days after surgery, prevented adhesion significantly. The IL‐22 receptor was induced on the mesothelial membrane, and IL‐22BP, an inhibitor of IL‐22, was reduced 3 days after surgery. Furthermore, IFN‐γ was identified to have the ability to induce IL‐22R, and IL‐18, which was induced by the infiltrating macrophages, was found to inhibit IL‐22BP expression both in vivo and in vitro. Together, these data suggest that IL‐22 may promote adhesion formation and that the regulation of IL‐22, IL‐22R, and IL‐22BP may have therapeutic potential to prevent adhesion formation after surgery without disturbing the normal immune process.
Δεν υπάρχουν σχόλια:
Δημοσίευση σχολίου