PURPOSE OF REVIEW: The pathophysiological riddle of the clinically important postoperative ileus (POI) has been solved more and more over the last decade. The POI is caused by inflammation and paralysis at the manipulated site propagating to the entire, unmanipulated gastrointestinal tract. Intestinal macrophages produce mediators that paralyze myocytes, but it is unclear how macrophages are activated, particularly those in unmanipulated areas. In addition to direct or neurally mediated activation of intestinal macrophages, a new immunologically mediated activation has been proposed. RECENT FINDINGS: Recently, it has been shown that the surgical trauma induces interleukin-12 (IL-12) production by intestinal dendritic cells, which activates TH1-memory cells at the manipulated site. Those TH1-memory cells produce interferon-γ (IFN-γ). Those TH1 CCR9 cells also migrate to unmanipulated parts of the gastrointestinal tract. Their IFN-γ stimulates intestinal macrophages to produce nitirc oxide paralyzing myocytes leading to gastrointestinal hypomotility. SUMMARY: The involvement of the adaptive (T-helper type 1 cell-mediated immune response) and of the innate (mast cells, intestinal macrophages) immune system in the pathophysiology of POI displays possible targets for objective monitoring and treatment of POI.
PURPOSE OF REVIEW: The pathophysiological riddle of the clinically important postoperative ileus (POI) has been solved more and more over the last decade. The POI is caused by inflammation and paralysis at the manipulated site propagating to the entire, unmanipulated gastrointestinal tract. Intestinal macrophages produce mediators that paralyze myocytes, but it is unclear how macrophages are activated, particularly those in unmanipulated areas. In addition to direct or neurally mediated activation of intestinal macrophages, a new immunologically mediated activation has been proposed. RECENT FINDINGS: Recently, it has been shown that the surgical trauma induces interleukin-12 (IL-12) production by intestinal dendritic cells, which activates TH1-memory cells at the manipulated site. Those TH1-memory cells produce interferon-γ (IFN-γ). Those TH1 CCR9 cells also migrate to unmanipulated parts of the gastrointestinal tract. Their IFN-γ stimulates intestinal macrophages to produce nitirc oxide paralyzing myocytes leading to gastrointestinal hypomotility. SUMMARY: The involvement of the adaptive (T-helper type 1 cell-mediated immune response) and of the innate (mast cells, intestinal macrophages) immune system in the pathophysiology of POI displays possible targets for objective monitoring and treatment of POI.
Authors: Sjoerd H W van Bree; Andrea Nemethova; Cathy Cailotto; Pedro J Gomez-Pinilla; Gianluca Matteoli; Guy E Boeckxstaens Journal: Nat Rev Gastroenterol Hepatol Date: 2012-07-17 Impact factor: 46.802
Authors: Sisi Lin; Florian Kühn; Tobias S Schiergens; Andrey A Zamyatnin; Orkhan Isayev; Eldar Gasimov; Jens Werner; Yongyu Li; Alexandr V Bazhin Journal: Int J Med Sci Date: 2021-06-16 Impact factor: 3.738