• Title/Summary/Keyword: alveolar air

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Epidemic acute interstitial pneumonia in children occurred during the early 2006s (2006년 초에 유행한 소아 급성 간질성폐렴)

  • Cheon, Chong Kun;Jin, Hyun-Seung;Kang, Eun Kyeong;Kim, Hyo Bin;Kim, Byoung-Joo;Yu, Jinho;Park, Seong Jong;Hong, Soo-Jong;Park, June Dong
    • Clinical and Experimental Pediatrics
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    • v.51 no.4
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    • pp.383-390
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    • 2008
  • Purpose : This study was aimed to analyze the clinical characteristics of patients with acute interstitial pneumonia who had presented similar clinical patterns from March to June, 2006 and to describe our experience of treatment and to identify risk factors associated with prognosis. Methods : The clinical characteristics, radiologic and histopathologic findings and response to steroids of 15 patients (non-survival group [n=7] and survival group [control, n=8]) with acute interstitial pneumonia were investigated through the review of medical records. Results : The mean age of the patients was 26 (range: 3-48) months. Cough, cyanosis and fever were frequent symptoms. The most frequent radiologic findings on admission were pneumomediastium and extensive ground glass opacity. Surgical lung biopsy was performed on 8/15 (53.3%) patients and diffuse alveolar damage was found. Mechanical ventilation was applied for 9/15 (60.0%) patients for 40 (range: 1-99) days. Five patients in survival group received steroid treatment and 7 patients in non-survivial group (P=0.20). One patient in survival group received steroid pulse treatment and 4 patients in non-survival group (P=0.12). Seven patients died all of respiratory failure. The survival rate was 53.4%. Conclusion : The patients with acute interstitial pneumonia which occurred on spring 2006 showed high mortality because of rapidly and extensively progressing pulmonary fibrosis and air leakage. Therefore, we should consider surgical lung biopsy and steroid application earlier. We should recognize this acute interstitial pneumonia occurring on spring in domestics and need to investigate the cause and treatment in large scale.

The Induction of ROS-dependent Autophagy by Particulate Matter 2.5 and Hydrogen Peroxide in Human Lung Epithelial A549 Cells (미세먼지와 산화적 스트레스에 의한 인간 폐 상피 A549 세포에의 ROS 의존적 자가포식 유도)

  • Park, Beom Su;Kim, Da Hye;Hwangbo, Hyun;Lee, Hyesook;Hong, Su Hyun;Cheong, Jaehun;Choi, Yung Hyun
    • Journal of Life Science
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    • v.32 no.4
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    • pp.310-317
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    • 2022
  • Recently, interest in the harmful factors of particulate matter (PM), a major component of air pollution, has been increasing. In particular, PM2.5 with a diameter of less than 2.5 ㎛ is well known to induce oxidative stress accompanied by autophagy in human lung epithelial cells. However, studies on whether PM2.5 increases autophagy under oxidative stress and whether this process is reactive oxygen species (ROS)-dependent are insufficient. Therefore, in this study, we investigated whether PM2.5 promotes autophagy through the generation of ROS in human alveolar epithelial A594 cells. According to our results, cells co-treated with PM2.5 and hydrogen peroxide (H2O2) showed a lower cell viability than cells treated with each alone, which was associated with increased total and mitochondrial ROS production. The co-treatment of PM2.5 and H2O2 also increased autophagy induction, which was confirmed through Cyto-ID staining, and the expression of autophagy biomarker proteins increased. However, when ROS generation was artificially blocked by N-acetyl-L-cysteine pretreatment, the reduction in cell viability and induction of autophagy by PM2.5 and H2O2 co-treatment were markedly attenuated. Therefore, the present results suggest that PM2.5-induced ROS generation may play a critical role in autophagy induction in A549 cells.