Mice deficient in myeloperoxidase and phagocyte NADPH oxidase exacerbates lung inflammation induced by zymosan and nonviable Candida albicans

2014 Fiscal Year Final Research Report

• Project/Area Number: 23580406
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Basic veterinary science/Basic zootechnical science
• Research Institution: Yokohama City University
• Principal Investigator: ARATANI YASUAKI 横浜市立大学, 生命ナノシステム科学研究科, 教授 (30192470)
• Project Period (FY): 2011-04-28 – 2015-03-31
• Keywords: 免疫 / 炎症 / 好中球 / 活性酸素 / ミエロペルオキシダーゼ

Outline of Final Research Achievements

Neutrophil accumulation is a critical event in the pathogenesis of lung inflammation. Myeloperoxidase (MPO) and phagocyte NADPH oxidase, major constituents of neutrophils that generate reactive oxygen species (ROS), contribute to microbial killing. This study examined the role of these enzymes in neutrophil recruitment into the zymozan- or nonviable Candida albicans (nCA)-exposed lung of mice. Mice deficient in MPO and phagocyte NADPH oxidase that pulmonary received zymosan and nCA showed more severe pneumonia than wild-type mice. This was associated with higher levels of several inflammatory mediators in the lungs of these mutant mice. Enhanced production of chemokine by the mutant neutrophils, concomitant with up-regulation of Syk/ERK/NF-kB pathway, may at least partly contribute to exacerbated inflammation in the mutant mice. Thus, loss of ROS production by neutrophils causes significant abnormalities in both host defense and inflammation.

Free Research Field

免疫生物学