Intravenous immunoglobulin enhances the killing activity and autophagy of neutrophils isolated from immunocompromised patients against multidrug-resistant bacteria
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説明
Intravenous immunoglobulin (IVIG) is periodically administered to immunocompromised patients together with antimicrobial agents. The evidence that supports the effectiveness of IVIG is mostly based on data from randomized clinical trials; the underlying mechanisms are poorly understood. A recent study revealed that killing of multidrug-resistant bacteria and drug-sensitive strains by neutrophils isolated from healthy donors is enhanced by an IVIG preparation. However, the effectiveness of IVIG in immunocompromised patients remains unclear. The present study found that IVIG increased both killing activity and O2(-) release by neutrophils isolated from six patients receiving immune-suppressive drugs after hematopoietic stem cell transplantation (HSCT); these neutrophils killed both multidrug-resistant extended-spectrum β-lactamase-producing Escherichia coli (E. coli) and multidrug-resistant Pseudomonas aeruginosa (P. aeruginosa). Moreover, IVIG increased the autophagy of the neutrophils, which is known to play an important role in innate immunity. These results suggest that IVIG promotes both the killing activity and autophagy of neutrophils isolated from immunocompromised patients against multidrug-resistant bacteria.
収録刊行物
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- Biochemical and Biophysical Research Communications
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Biochemical and Biophysical Research Communications 464 (1), 94-99, 2015-08
Elsevier BV
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キーワード
- Adult
- Male
- Neutrophils
- Primary Cell Culture
- Microbial Sensitivity Tests
- beta-Lactamases
- Immunocompromised Host
- Superoxides
- Drug Resistance, Multiple, Bacterial
- Autophagy
- Escherichia coli
- Humans
- Hematopoietic Stem Cell Transplantation
- Immunoglobulins, Intravenous
- Middle Aged
- Coculture Techniques
- Anti-Bacterial Agents
- Hematologic Neoplasms
- Pseudomonas aeruginosa
- Female
- Immunosuppressive Agents
詳細情報 詳細情報について
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- CRID
- 1360283690800107136
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- ISSN
- 0006291X
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- PubMed
- 26119690
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- 資料種別
- journal article
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- データソース種別
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- Crossref
- KAKEN
- OpenAIRE