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Title: Enhanced generation of reactive oxygen species by interferon-γ may have contributed to successful treatment of invasive pulmonary aspergillosis in a patient with chronic granulomatous disease.
Authors: Yamashita, Kouhei
Miyoshi, Takashi
Arai, Yasuyuki  kyouindb  KAKEN_id  orcid https://orcid.org/0000-0002-9662-5093 (unconfirmed)
Mizugishi, Kiyomi
Takaori-Kondo, Akifumi
Ueyama, Takehiko
Author's alias: 山下, 浩平
Keywords: Chronic granulomatous disease
Invasive pulmonary aspergillosis
Interferon-γ
Reactive oxygen species
Voriconazole
Issue Date: 24-Mar-2013
Publisher: Springer Japan
Journal title: International journal of hematology
Volume: 97
Issue: 4
Start page: 505
End page: 510
Abstract: Invasive pulmonary aspergillosis (IPA) is a life-threatening complication of chronic granulomatous disease (CGD), a rare inherited disorder of phagocytes that is characterized by a defect in the production of reactive oxygen species (ROS) caused by mutations in NADPH oxidase 2. Here, we report a case of successful treatment of IPA complicated with CGD by the administration of interferon-γ (IFN-γ) in combination with voriconazole. The patient carried a splice site mutation in the CYBB gene, and the neutrophils could produce a certain amount of ROS. In this case, augmentation of ROS generation in the patient's neutrophils was observed after in vivo IFN-γ treatment, which may be attributable to the induction of a normal CYBB gene in the myeloid progenitor cells. This treatment, in combination with voriconazole, may have contributed to the reversal of IPA in this patient. These results suggest that the in vivo use of IFN-γ may augment ROS generation in CGD neutrophils, thus leading to the successful treatment of severe IPA.
Rights: The final publication is available at Springer via http://dx.doi.org/10.1007/s12185-013-1315-y
この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。
This is not the published version. Please cite only the published version.
URI: http://hdl.handle.net/2433/196751
DOI(Published Version): 10.1007/s12185-013-1315-y
PubMed ID: 23526099
Appears in Collections:Journal Articles

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