2012 Fiscal Year Final Research Report
Mechanism of hyperinflammation in chronic granulomatous disease: mouse iPS cells expressing human gp91phox
| Project/Area Number |
22791021
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Pediatrics
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| Research Institution | National Research Institute for Child Health and Development |
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Principal Investigator |
KAWAI Toshinao 独立行政法人国立成育医療研究センター, 成育遺伝研究部, 室長 (20328305)
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| Project Period (FY) |
2010 – 2012
|
| Keywords | 小児免疫 / アレルギー / 膠原病学 |
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| Research Abstract |
We investigated an underlying mechanisms of excessive inflammation in patients with chronic granulomatous disease. Our data suggested that reactive oxygen species generated by NADPH oxidase suppressed the lipopolysaccharide-induced inflammatory cytokine production through NLRP3 inflammasome and NF_κB signaling pathway in monocytes that play a central role of immune response. Although further works are required to clarify the mechanisms of excessive inflammation in CGD patients, this data indicates that reduction of reactive oxygen species generated by NADPH oxidase would induce dysregulated production of inflammatory cytokines.
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