2012 Fiscal Year Final Research Report
The pathophysiology of intratracheal LPS or BLM lung injury mice model after LPS-priming
| Project/Area Number |
22590854
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Shinshu University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
YOKOYAMA Toshiki 信州大学, 医学部附属病院, 助教 (20467161)
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| Project Period (FY) |
2010 – 2012
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| Keywords | LPS 肺損傷 / LPS プライミング / ブレオマイシン |
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| Research Abstract |
To examine potential roles for alveolar macrophages (AM) in the priming response in model of acute lung injury (ALI), primed WT mice were treated with Cl2MDP-liposome (depleted primed AM) on day -3 followed by IT． By day 5, the non-depleted primed group exhibited reduced bronchoalveolar lavage (BAL) protein and BAL cells compared to depleted primed AM group. Lung histology revealed nearly complete resolution of injury on day 5 in non-AM-depleted primed group; interstitial thickening and lung consolidation persisted in the AM-depleted primed group. Flow cytometry revealed thatat day 0 over 90% of AMs were depleted in the Cl2MDP-liposome treated group. BAL tumor necrosis factor-alpha was lower on day 1 and was higher on day 5 in depleted primed AM group compared to non-depleted primed AM group while BAL IL-10 was higher in non-depleted primed AM group on day 1 after LPS. In contrast to primed WT mice, IL-10-null mice did not exhibit accelerated resolution of lung injury with priming. These studies implicate AM-derived IL-10 in the accelerated resolution of ALI produced by LPS priming. Definition of mechanisms related to priming could provide important insights into potential new therapies for ALI..
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