Apoptosis inhibitor of macrophage ameliorates fungus-induced peritoneal injury model in mice

Abstract Fungal peritonitis in a patient on peritoneal dialysis (PD) is a refractory injury accompanied by severe inflammation, predisposing patients to a poor prognosis. Defective clearance of necrotic tissue interferes with amelioration of tissue injury and induces abnormal tissue remodeling. In t...

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Autores principales:	Takako Tomita, Satoko Arai, Kento Kitada, Masashi Mizuno, Yasuhiro Suzuki, Fumiko Sakata, Daisuke Nakano, Emiri Hiramoto, Yoshifumi Takei, Shoichi Maruyama, Akira Nishiyama, Seiichi Matsuo, Toru Miyazaki, Yasuhiko Ito
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/364c8f1dadb54640b28a132ca89030fc
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spelling	oai:doaj.org-article:364c8f1dadb54640b28a132ca89030fc2021-12-02T11:53:00ZApoptosis inhibitor of macrophage ameliorates fungus-induced peritoneal injury model in mice10.1038/s41598-017-06824-62045-2322https://doaj.org/article/364c8f1dadb54640b28a132ca89030fc2017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-06824-6https://doaj.org/toc/2045-2322Abstract Fungal peritonitis in a patient on peritoneal dialysis (PD) is a refractory injury accompanied by severe inflammation, predisposing patients to a poor prognosis. Defective clearance of necrotic tissue interferes with amelioration of tissue injury and induces abnormal tissue remodeling. In the recent reports, apoptosis inhibitor of macrophage (AIM, also called CD5L) prevents obesity, hepatocellular carcinoma and acute kidney injury. Here, we investigated potential roles of AIM in prevention of progression of fungal peritonitis models. AIM −/− mice subjected to zymosan-induced peritonitis exhibited progressive inflammation and sustained peritoneal necrosis tissue on day 28 after the disease induction, whereas there was an improvement in AIM +/+ mice. This appeared to be caused by deposition of AIM at the necrotic peritoneum in AIM +/+ mice. In vitro, AIM enhanced the engulfment of necrotic debris by macrophages derived from zymosan-induced peritonitis, M1- and M2a-like bone marrow derived macrophages, as well as by mesothelial cells. In addition, administration of recombinant AIM dramatically ameliorated severe inflammation associated with necrosis in zymosan-induced peritonitis of AIM −/− mice. Our observations suggest that AIM appears to be involved in the repair process of zymosan-induced peritonitis, and thus, could be the basis of development of new therapeutic strategies for PD-related fungal peritonitis.Takako TomitaSatoko AraiKento KitadaMasashi MizunoYasuhiro SuzukiFumiko SakataDaisuke NakanoEmiri HiramotoYoshifumi TakeiShoichi MaruyamaAkira NishiyamaSeiichi MatsuoToru MiyazakiYasuhiko ItoNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-14 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Takako Tomita Satoko Arai Kento Kitada Masashi Mizuno Yasuhiro Suzuki Fumiko Sakata Daisuke Nakano Emiri Hiramoto Yoshifumi Takei Shoichi Maruyama Akira Nishiyama Seiichi Matsuo Toru Miyazaki Yasuhiko Ito Apoptosis inhibitor of macrophage ameliorates fungus-induced peritoneal injury model in mice
description	Abstract Fungal peritonitis in a patient on peritoneal dialysis (PD) is a refractory injury accompanied by severe inflammation, predisposing patients to a poor prognosis. Defective clearance of necrotic tissue interferes with amelioration of tissue injury and induces abnormal tissue remodeling. In the recent reports, apoptosis inhibitor of macrophage (AIM, also called CD5L) prevents obesity, hepatocellular carcinoma and acute kidney injury. Here, we investigated potential roles of AIM in prevention of progression of fungal peritonitis models. AIM −/− mice subjected to zymosan-induced peritonitis exhibited progressive inflammation and sustained peritoneal necrosis tissue on day 28 after the disease induction, whereas there was an improvement in AIM +/+ mice. This appeared to be caused by deposition of AIM at the necrotic peritoneum in AIM +/+ mice. In vitro, AIM enhanced the engulfment of necrotic debris by macrophages derived from zymosan-induced peritonitis, M1- and M2a-like bone marrow derived macrophages, as well as by mesothelial cells. In addition, administration of recombinant AIM dramatically ameliorated severe inflammation associated with necrosis in zymosan-induced peritonitis of AIM −/− mice. Our observations suggest that AIM appears to be involved in the repair process of zymosan-induced peritonitis, and thus, could be the basis of development of new therapeutic strategies for PD-related fungal peritonitis.
format	article
author	Takako Tomita Satoko Arai Kento Kitada Masashi Mizuno Yasuhiro Suzuki Fumiko Sakata Daisuke Nakano Emiri Hiramoto Yoshifumi Takei Shoichi Maruyama Akira Nishiyama Seiichi Matsuo Toru Miyazaki Yasuhiko Ito
author_facet	Takako Tomita Satoko Arai Kento Kitada Masashi Mizuno Yasuhiro Suzuki Fumiko Sakata Daisuke Nakano Emiri Hiramoto Yoshifumi Takei Shoichi Maruyama Akira Nishiyama Seiichi Matsuo Toru Miyazaki Yasuhiko Ito
author_sort	Takako Tomita
title	Apoptosis inhibitor of macrophage ameliorates fungus-induced peritoneal injury model in mice
title_short	Apoptosis inhibitor of macrophage ameliorates fungus-induced peritoneal injury model in mice
title_full	Apoptosis inhibitor of macrophage ameliorates fungus-induced peritoneal injury model in mice
title_fullStr	Apoptosis inhibitor of macrophage ameliorates fungus-induced peritoneal injury model in mice
title_full_unstemmed	Apoptosis inhibitor of macrophage ameliorates fungus-induced peritoneal injury model in mice
title_sort	apoptosis inhibitor of macrophage ameliorates fungus-induced peritoneal injury model in mice
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/364c8f1dadb54640b28a132ca89030fc
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Apoptosis inhibitor of macrophage ameliorates fungus-induced peritoneal injury model in mice

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