2022 Fiscal Year Final Research Report
The study on Immunosenescence in Chronic Obstructive Pulmonary Disease
| Project/Area Number |
18K08188
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 53030:Respiratory medicine-related
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| Research Institution | Akita University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
荒屋 潤 東京慈恵会医科大学, 医学部, 教授 (90468679)
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| Project Period (FY) |
2018-04-01 – 2023-03-31
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| Keywords | COPD / 細胞老化 / 酸化ストレス / 肺胞マクロファージ / 体表肺エコー検査 |
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| Outline of Final Research Achievements |
To validate cellular senescence and chronic inflammation in COPD, we examined the expression of senescence-related factors (PARK2, LaminB1, NCOA4) in peripheral blood and the expression of innate immune system agonist molecules (ADMATS20, SPHK2, TNFSF14) by CSE stimuli to alveolar MF, but no significant trends were obtained. On the other hand, a significant association between the number of i-ULCs by body surface lung ultrasonography and lung function decline was demonstrated for interstitial pneumonia, which is related to smoking and cellular senescence, and statin stimulation of HBECs induced the expression of the antioxidant stressor HO-1. From the latter, an investigation of anti-aging effects of statin on airway epithelium is planned. Due to the COVID-19 disaster in the study period, difficulties were encountered in specimen collection. We obtained basic data that are expected to be validated and developed.
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| Free Research Field |
呼吸器内科
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| Academic Significance and Societal Importance of the Research Achievements |
COPDでの細胞内老化関連因子を末血ELISAで簡易に評価することは難しいことが示された。また、肺胞MFへの喫煙刺激による自然免疫系作動分子発現は一様ではなく基礎疾患により変動することが示された。免疫系も含めた細胞老化の評価の簡易化はまだ難しく、個々の症例で細胞種の違いも勘案して検討することが必要である。
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