| Project/Area Number |
22790959
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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 |
Infectious disease medicine
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| Research Institution | National Institute of Infectious Diseases |
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Principal Investigator |
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| Project Period (FY) |
2010-04-01 – 2014-03-31
|
| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| Keywords | 感染症防御学 / 劇症型溶血性レンサ球菌感染症 / IFN-γ / 感染症 / 細菌 / 免疫学 / 未成熟骨髄系細胞 |
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| Research Abstract |
Cytokine-activated neutrophils are known to be essential for protection against group A Streptococcus (GAS) infections. However, during severe invasive GAS infections that accompanied with neutropenia, it remains unclear which factors are protective against such infections, and which cell population is the source of them. Here we show that mice infected with severe invasive GAS isolates, but not with non-invasive GAS isolates, exhibit high concentrations of plasma IFN-g during the early stage of infection. IFN-g is necessary to protect mice, and is produced by a novel population of GM-CSF-dependent immature myeloid cells with ring-shaped nuclei (IFN-g-producing immature myeloid cells; gIMCs). These gIMCs express monocyte and granulocyte markers, and also produce nitric oxide. The adoptive transfer of gIMCs ameliorates infection in wild-type and IFN-g-deficient mice. Our results indicate that gIMCs have a protective role during the early stage of severe invasive GAS infections.
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