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

Nature communications (2021-04-16)
Tomoya Ito, Yusuke Shintani, Laura Fields, Manabu Shiraishi, Mihai-Nicolae Podaru, Satoshi Kainuma, Kizuku Yamashita, Kazuya Kobayashi, Mauro Perretti, Fiona Lewis-McDougall, Ken Suzuki
ZUSAMMENFASSUNG

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 F4/80HighCD206- 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.

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DAPI, for nucleic acid staining
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Anti-Laminin in Kaninchen hergestellte Antikörper, 0.5 mg/mL, affinity isolated antibody, buffered aqueous solution
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Eosin-Y-Lösung, alkoholisch
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Mayers Hämatoxylin-Lösung
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Duolink® In Situ Orange Starter Kit Goat/Rabbit