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博士論文 / IL-17A contributes to reducing IFN-γ/IL-4 ratio and persistence of Entamoeba histolytica during intestinal amebiasis IL-17Aは赤痢アメーバの腸管感染においてIFN-γ/IL-4比の減少と持続感染に寄与する

著者

書誌事項

タイトル

IL-17A contributes to reducing IFN-γ/IL-4 ratio and persistence of Entamoeba histolytica during intestinal amebiasis

タイトル別名

IL-17Aは赤痢アメーバの腸管感染においてIFN-γ/IL-4比の減少と持続感染に寄与する

著者名

Deloer Sharmina

学位授与大学

Nagasaki University (長崎大学) (大学ID:0073) (CAT機関ID:KI000877)

取得学位

博士(医学)

学位授与番号

甲医歯薬第1005号

学位授与年月日

2017-12-06

注記・抄録

Amebiasis is an infectious disease caused by Entamoeba histolytica, an anaerobic protozoan parasite, and is a major public health problem worldwide, particularly in areas with inadequate sanitation and poor hygiene. Th1 responses, represented by interferon gamma (IFN-γ), play a protective role by clearing the amebae from the gut, whereas Th2 responses are responsible for chronic infection. Th17 responses preconditioned by vaccination or by modulating the intestinal microbiome protect mice from the settlement of E. histolytica. However, the role of interleukin-17A (IL-17A), which is upregulated during the natural course of intestinal amebiasis, has not been clarified. The aim of this study was to investigate the role of IL-17A during intestinal amebiasis in a mouse model. IL-17A knockout and wild-type CBA/J mice were challenged intracecally with 2 × 106 E. histolytica trophozoites, and their infection, pathology, and immune responses were monitored. Neither the initial settlement of E. histolytica nor the inflammation of the cecum was affected by the absence of IL-17A for week 1, but the infection rate and parasite burden declined in a late stage of infection, accompanied by an increased IFN-γ/IL-4 ratio. Therefore, IL-17A contributes to the persistence of E. histolytica and modulates the immune response, including the IFN-γ/IL-4 ratio, which may be responsible for the reduction of the parasite burden in the IL-17A knockout mice during the chronic phase of intestinal amebiasis.

開始ページ : 817

終了ページ : 823

元資料の権利情報 : © 2017 Elsevier B.V. All rights reserved.

各種コード

NII論文ID(NAID)

500001054910

NII著者ID(NRID)
  • 8000001159397
DOI (出版社)

10.1016/j.parint.2017.09.011

DOI

info:doi/10.1016/j.parint.2017.09.011

本文言語コード

eng

データ提供元

機関リポジトリ / NDLデジタルコレクション

DOI

博士論文 / 長崎大学 / 医学

博士論文 / 長崎大学

博士論文 / 医学

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