Cell barrier function of resident peritoneal macrophages in post-operative adhesions

Post-operative adhesions are a leading cause of abdominal surgery-associated morbidity. Exposed fibrin clots on the damaged peritoneum, in which the mesothelial barrier is disrupted, readily adhere to surrounding tissues, resulting in adhesion formation. Here we show that resident F4/80(High)CD206(-) peritoneal macrophages promptly accumulate on the lesion and form a 'macrophage barrier' to shield fibrin clots in place of the lost mesothelium in mice. Depletion of this macrophage subset or blockage of CD11b impairs the macrophage barrier and exacerbates adhesions. The macrophage barrier is usually insufficient to fully preclude the adhesion formation; however, it could be augmented by IL-4-based treatment or adoptive transfer of this macrophage subset, resulting in robust prevention of adhesions. By contrast, monocyte-derived recruited peritoneal macrophages are not involved in the macrophage barrier. These results highlight a previously unidentified cell barrier function of a specific macrophage subset, also proposing an innovative approach to prevent post-operative adhesions. Peritoneal adhesions are a major cause of complications after abdominal surgery. Here the authors use a post-operative abdominal adhesion model in mice to show that resident F4/80(High)CD206(-) macrophages form a protective barrier that can be enhanced by IL-4 administration or adoptive transfer of these cells.

Automated summary

Peritoneal adhesions are a common complication after abdominal surgery. Research shows that a specific subset of F4/80(High)CD206(-) macrophages can form a protective barrier to prevent adhesion formation, which can be enhanced by IL-4 treatment or cell transfer.