JaLCDOI 10.18926/AMO/32852
フルテキストURL fulltext.pdf
著者 Iio, Kouji| Iio, Tomoe Ueno| Okui, Yuhei| Ichikawa, Hirohisa| Tanimoto, Yasushi| Miyahara, Nobuaki| Kanehiro, Arihiko| Tanimoto, Mitsune| Nakata, Yasunari| Kataoka, Mikio|
抄録

Propionibacterium acnes has been implicated as an etiologic agent of sarcoidosis since the isolation of this bacterium from sarcoid lesions. We experimentally produced a murine pulmonary granuloma model using P. acnes with several features that simulate sarcoidosis. Mice were sensitized with heat-killed P. acnes and complete Freund's adjuvant and were subsequently challenged with heat-killed P. acnes at 2-week intervals. P. acnes-challenged mice developed epitheloid cell granulomas in the lungs. These mice showed a pulmonary immune response characterized by an increased number of T-lymphocytes, especially CD4 cells, and the ratio of CD4/CD8 in bronchoalveolar lavage (BAL) fluid also increased. Furthermore, significant elevations in both angiotensin-converting enzyme (ACE) serum levels and antibody titers against P. acnes were observed. Mice sensitized with P. acnes without complete Freund's adjuvant were capable of forming pulmonary granulomas, which appeared to be caused by indigenous P. acnes. The genome of P. acnes was found in the lungs, BAL cells, hilar lymph nodes, liver, and spleen in non-sensitized mice, which were thought to be germ-free. These results suggest that the immune response against indigenous P. acnes may play an important role in the pathogenesis of granuloma formation in a murine model.

キーワード Propionibacterium acnes experimental granuloma sarcoidosis
Amo Type Original Article
出版物タイトル Acta Medica Okayama
発行日 2010-04
64巻
2号
出版者 Okayama University Medical School
開始ページ 75
終了ページ 83
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 英語
論文のバージョン publisher
査読 有り
PubMed ID 20424662
Web of Science KeyUT 000276996900001
JaLCDOI 10.18926/AMO/46635
フルテキストURL 65_3_215.pdf
著者 Waseda, Koichi| Tanimoto, Yasushi| Hasegawa, Kenjiro| Miyahara, Nobuaki| Nojima, Daisuke| Ikeda, Genyo| Kanehiro, Arihiko| Okada, Chiharu| Kimata, Yoshihiro| Tanimoto, Mitsune|
抄録 Churg-Strauss syndrome (CSS) is a granulomatous necrotizing vasculitis of unknown etiology associated with bronchial asthma. Despite affecting small to medium-sized vessels, necrosis of the digits due to vasculitis is extremely rare. We report a case of CSS with necrosis of the toe tips. A 37-year-old woman with asthma, who had been diagnosed with CSS 2 years ago, was admitted to our hospital with an exacerbation of CSS. The patient had a high grade fever and complained of abdominal pain and numbness of the lower extremities. Blood examination revealed marked eosinophilia. The fever pattern, abdominal pain and blood eosinophilia showed improvement by combination treatment with prednisolone and cyclophosphamide. However, the color of her right toe tips changed, and necrosis finally resulted despite antithrombotic therapy. Arteriography showed narrowing of the dorsalis pedis artery and of the more peripheral arteries of her right leg. Stump plasty with negative pressure dressing therapy for the toe tips, but not amputation, was done to preserve the leg function. While numbness of the extremities remained, no recurrence of necrosis was seen. Clinicians need to be aware that rare complications of CSS, including necrosis of the digits, can occur.
キーワード bronchial asthma Churg-Strauss syndrome eosinophilia necrosis of toe tips stump plasty
Amo Type Case Report
出版物タイトル Acta Medica Okayama
発行日 2011-06
65巻
3号
出版者 Okayama University Medical School
開始ページ 215
終了ページ 218
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 英語
著作権者 CopyrightⒸ 2011 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 21709721
Web of Science KeyUT 000292017500010
JaLCDOI 10.18926/AMO/47266
フルテキストURL 65_6_403.pdf
著者 Waseda, Koichi| Tanimoto, Yasushi| Ichiba, Shingo| Miyahara, Nobuaki| Murakami, Toshi| Ochi, Nobuaki| Terado, Michihisa| Nagano, Osamu| Maeda, Yoshinobu| Kanehiro, Arihiko| Ujike, Yoshihito| Tanimoto, Mitsune|
抄録 Bronchiolitis obliterans (BO) is a disease with a poor prognosis, and a key factor that limits long-term survival after allogeneic hematopoietic stem cell transplantation (HSCT). We here report a case of a 31-year woman with acute lymphatic leukemia, which was treated by chemotherapy and HSCT, and consequently developed BO 2 years after HSCT. A non-tuberculous mycobacterial infection occurred and showed gradual exacerbation. She started taking anti-mycobacterial drugs, but lost appetite, felt tired and finally lost consciousness one month after beginning medication. Arterial blood gas revealed marked hypercapnia. Using extracorporeal life support (ECLS), the carbon dioxide concentration was reduced and her consciousness recovered. To our knowledge, this is the first case in which ECLS was successfully used for hypercapnia in a patient with BO.
キーワード extracorporeal life support hypercapnia bronchiolitis obliterans noninvasive positive pressure ventilation
Amo Type Case Report
出版物タイトル Acta Medica Okayama
発行日 2011-12
65巻
6号
出版者 Okayama University Medical School
開始ページ 403
終了ページ 406
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 英語
著作権者 CopyrightⒸ 2011 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 22189481
Web of Science KeyUT 000298516900007
フルテキストURL fulltext20221223-3.pdf NA_Itano_Fig.pdf supl20221223-3.pdf NA_Itano_Supl.pdf
著者 Itano, Junko| Taniguchi, Akihiko| Senoo, Satoru| Asada, Noboru| Gion, Yuka| Egusa, Yuria| Guo, Lili| Oda, Naohiro| Araki, Kota| Sato, Yasuharu| Toyooka, Shinichi| Kiura, Katsuyuki| Maeda, Yoshinobu| Miyahara, Nobuaki|
キーワード idiopathic pulmonary fibrosis NPY IL-1 beta; bleomycin bronchial epithelial cells
備考 Originally Published in:Itano J, Taniguchi A, Senoo S, Asada N, Gion Y, Egusa Y, Guo L, Oda N, Araki K, Sato Y, Toyooka S, Kiura K, Maeda Y, Miyahara N. Neuropeptide Y Antagonizes Development of Pulmonary Fibrosis through IL-1β Inhibition. Am J Respir Cell Mol Biol. 2022 Dec;67(6):654-665.
DOI: 10.1165/rcmb.2021-0542OC
Copyright © 2022 by the American Thoracic Society
The final publication is available at https://doi.org/10.1165/rcmb.2021-0542OC |
This full-text will be available in Dec. 2023.|
発行日 2022-12
出版物タイトル American Journal of Respiratory Cell and Molecular Biology
67巻
6号
出版者 American Thoracic Society
開始ページ 654
終了ページ 665
ISSN 1044-1549
NCID AA10707251
資料タイプ 学術雑誌論文
言語 英語
OAI-PMH Set 岡山大学
著作権者 © 2022 by the American Thoracic Society
論文のバージョン author
PubMed ID 36122332
DOI 10.1165/rcmb.2021-0542oc
Web of Science KeyUT 000891796900010
関連URL isVersionOf https://doi.org/10.1165/rcmb.2021-0542oc
JaLCDOI 10.18926/AMO/54422
フルテキストURL 70_3_217.pdf
著者 Waseda, Koichi| Ocho, Kazuki| Hasegawa, Kou| Kimura, Kosuke| Iwamuro, Masaya| Hanayama, Yoshihisa| Kondo, Eisei| Miyahara, Nobuaki| Otsuka, Fumio|
抄録 KL-6 is a glycoprotein found predominantly on type II pneumocytes and alveolar macrophages, and often shows increased serum levels in patients with interstitial pneumonia. We report a case of mycobacterium avium complex (MAC) infection whose disease activity was correlated with KL-6 levels in serum. During treatment of rheumatoid arthritis (RA)-associated interstitial lung disease (ILD) with prednisolone, chest image findings improved in association with decreased KL-6 levels. Following tapering of prednisolone, chest image findings deteriorated again as levels of KL-6 increased, suggesting recurrence of RA-ILD. Bronchoscopic examination revealed active MAC infection. Treatment of MAC infection not only improved chest image findings but also decreased KL-6 levels in serum, suggesting that KL-6 was increased by active MAC infection by itself, not by recurrence of RA-ILD. To the best of our knowledge, this is the first documentation of KL-6 elevation in serum in association with active MAC infection.
キーワード KL-6 mycobacterium avium complex pulmonary nontuberculous mycobacterium infection rheumatoid arthritis-associated interstitial lung disease bronchial alveolar lavage
Amo Type Case Report
出版物タイトル Acta Medica Okayama
発行日 2016-06
70巻
3号
出版者 Okayama University Medical School
開始ページ 217
終了ページ 221
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 英語
著作権者 CopyrightⒸ 2016 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 27339212
Web of Science KeyUT 000379406100010
JaLCDOI 10.18926/AMO/66912
フルテキストURL 78_2_095.pdf
著者 Itano, Junko| Kiura, Katsuyuki| Maeda, Yoshinobu| Miyahara, Nobuaki|
抄録 The lungs are very complex organs, and the respiratory system performs the dual roles of repairing tissue while protecting against infection from various environmental stimuli. Persistent external irritation disrupts the immune responses of tissues and cells in the respiratory system, ultimately leading to respiratory disease. Neuropeptide Y (NPY) is a 36-amino-acid polypeptide and a neurotransmitter that regulates homeostasis. The NPY receptor is a seven-transmembrane-domain G-protein-coupled receptor with six subtypes (Y1, Y2, Y3, Y4, Y5, and Y6). Of these receptors, Y1, Y2, Y4, and Y5 are functional in humans, and Y1 plays important roles in the immune responses of many organs, including the respiratory system. NPY and the Y1 receptor have critical roles in the pathogenesis of asthma, chronic obstructive pulmonary disease, and idiopathic pulmonary fibrosis. The effects of NPY on the airway immune response and pathogenesis differ among respiratory diseases. This review focuses on the involvement of NPY in the airway immune response and pathogenesis of various respiratory diseases.
キーワード neuropeptide y Y1 receptor airway immune response bronchial epithelial cells respiratory disease
Amo Type Review
出版物タイトル Acta Medica Okayama
発行日 2024-04
78巻
2号
出版者 Okayama University Medical School
開始ページ 95
終了ページ 106
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 英語
著作権者 Copyright Ⓒ 2024 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 38688827