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Original research
Altered distribution, activation and increased IL-17 production of mucosal-associated invariant T cells in patients with acute respiratory distress syndrome
  1. Tae-Ok Kim1,
  2. Ki-Jeong Park2,
  3. Young-Nan Cho2,
  4. Hye-Mi Jin2,
  5. Young-Goun Jo3,
  6. Hyo Shin Kim3,
  7. Jae Kyun Ju3,
  8. Hong-Joon Shin1,
  9. Bo-Gun Kho1,
  10. Seung-Jung Kee4,
  11. Yong-Wook Park2,5
  1. 1Pulmonology, Chonnam National University Medical School and Hospital, Gwangju, Korea
  2. 2Rheumatology, Chonnam National University Medical School and Hospital, Gwangju, Korea
  3. 3Surgery, Chonnam National University Medical School and Hospital, Gwangju, Korea
  4. 4Laboratory Medicine, Chonnam National University Medical School and Hospital, Gwangju, Korea
  5. 5Rheumatology, Chonnam National University Bitgoeul Hospital, Gwangju, Korea
  1. Correspondence to Professor Yong-Wook Park, Rheumatology, Chonnam National University Medical School and Hospital, Gwangju, South Korea; parkyw{at}jnu.ac.kr; Professor Seung-Jung Kee, Laboratory Medicine, Chonnam National University Medical School and Hospital, Gwangju, South Korea; sjkee{at}jnu.ac.kr

Abstract

Objective Mucosal-associated invariant T (MAIT) cells are a subset of innate-like T cells that are engaged in a number of diseases, but their roles in acute respiratory distress syndrome (ARDS) are not fully examined yet. This study aimed to examine levels and functions of MAIT cells in patients with ARDS.

Methods Peripheral blood samples from patients with ARDS (n=50) and healthy controls (HCs, n=50) were collected. Levels of MAIT cells, cytokines, CD69, programmed cell death-1 (PD-1) and lymphocyte-activation gene 3 (LAG-3) were measured by flow cytometry.

Results Circulating MAIT cell levels were significantly reduced in patients with ARDS than in HCs. MAIT cell levels were inversely correlated with disease severity and mortality. Cytokine production profiles in MAIT cells showed that percentages of interleukin (IL)-17 producing MAIT cell were significantly higher in patients with ARDS than in HCs. Patients with ARDS exhibited higher expression levels of CD69, PD-1 and LAG-3 in circulating MAIT cells. Moreover, levels of MAIT cells and expression levels of CD69, PD-1 and IL-17 in MAIT cells were higher in bronchoalveolar lavage fluid samples than in peripheral blood samples. Our in vitro experiments showed that MAIT cells triggered macrophages to produce proinflammatory cytokines such as tumour necrosis factor-α, IL-1β and IL-8.

Conclusions This study demonstrates that circulating MAIT cells are numerically deficient in patients with ARDS. In addition, MAIT cells were found to be activated, migrate into lung, secrete IL-17 and then stimulate macrophages. These findings suggest that MAIT cells contribute to the worsening of inflammation in the lung of patients with ARDS.

  • ARDS
  • critical care
  • cytokine biology
  • innate immunity

Data availability statement

Data are available upon reasonable request. All data relevant to the study are included in the article or uploaded as supplementary information. No data are available.

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Data availability statement

Data are available upon reasonable request. All data relevant to the study are included in the article or uploaded as supplementary information. No data are available.

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Footnotes

  • T-OK, K-JP and Y-NC are joint first authors.

  • T-OK, K-JP and Y-NC contributed equally.

  • Contributors T-OK, K-JP, Y-NC, H-MJ, Y-GJ, HSK, JKJ, S-JK and Y-WP designed this study, collected clinical information, analysed raw data, performed statistical analysis and contributed to writing of the paper. T-OK, K-JP, Y-NC and H-MJ performed experiments. Y-WP accepts full responsibility for the work and/or the conduct of the study, had access to the data, and controlled the decision to publish. All authors read and approved the final version of the manuscript.

  • Funding This study was supported by the National Research Foundation of Korea (2019R1A2C1003238, 2019R1F1A1059600, 2018R1A6A3A11042850) and the Chonnam National University Hospital Biomedical Research Institute (CRI18042-22).

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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