LAUSR

Simple Summary Patients with acute respiratory distress syndrome (ARDS) have high mortality. It is important to understand the complex immune interactions in ARDS, which may help identify potential therapeutic targets. In this study, we tried to determine the trends of human leukocyte antigen (HLA)-DR and cytokine expression in alveolar monocytes in patients with pneumonia-related ARDS. We found that alveolar monocyte HLA-DR expression (mHLA-DR) in survivors increased remarkably after seven days, and alveolar monocyte IL-10 expression in survivors decreased substantially after seven days. These findings highlighted the importance of serial increases in HLA-DR expression and decreases in IL-10 expression in alveolar monocytes of survivors. Abstract ARDS is a potentially lethal syndrome. HLA-DR expression in monocytes reflects their activation and antigen-presenting capacity. However, the correlation between clinical outcomes and HLA-DR expression in alveolar monocytes/macrophages in patients with pneumonia-related ARDS remains unclear. Thus, we determined the trends of HLA-DR and cytokine expressions in alveolar monocytes using repeated measurements to answer this question. Thirty-one pneumonia patients with respiratory failure and ARDS without coronavirus disease 2019 between November 2019 and November 2021 were enrolled in our intensive care unit and three without complete data were excluded. Interleukin (IL)-10, IL-12, and HLA-DR expression in bronchoalveolar lavage (BAL) monocytes were determined on days one and eight. Monocyte HLA-DR expression (mHLA-DR) and CD4 T lymphocytes percentages in BAL cells of survivors increased remarkably after seven days. Monocyte IL-10 expression and monocytes percentages in BAL cells of survivors decreased substantially after seven days. The mHLA-DR was negatively correlated with disease severity scores on day one and eight. In conclusion, serial increases in HLA-DR expression and decreases in IL-10 expression were observed in BAL monocytes of survivors of pneumonia-related ARDS. More studies are needed to confirm this point of view, and then development of a therapeutic agent restoring mHLA-DR and preventing IL-10 production can be considered.