Lower respiratory tract microbiota is associated with inflammation and hospital mortality in acute respiratory distress syndrome: a pilot study
CCCF ePoster library. Kyo M. 11/13/19; 283388; EP121 Disclosure(s): This work was supported by KAKENHI Grants from the Japan Society for the Promotion of Science (JSPS) (numbers JP 18K16518).
Dr. Michihito Kyo
Dr. Michihito Kyo
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Topic: Retrospective or Prospective Cohort Study or Case Series

Kyo, Michihito1; Nishioka, Keisuke2; Nakaya, Takaaki2; Kida, Yoshiko1; Tanabe, Yuko1; Ohshimo, Shinichiro1; Shime Nobuaki1
1 Department of Emergency and Critical Care Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan; 2 Department of Infectious Diseases, Kyoto Prefectural University of Medicine, Kyoto, Japan

INTRODUCTION: The lung microbiome maintains the homeostasis of the immune system within the lungs. In acute respiratory distress syndrome (ARDS), the lung microbiome is enriched with gut-derived bacteria; however, the specific microbiome associated with morbidity and mortality in patients with ARDS remains unclear.
OBJECTIVES: This study investigated the specific patterns of the lung microbiome that are correlated with mortality in ARDS patients.
METHODS: We analyzed the lung microbiome from the bronchoalveolar lavage fluid (BALF) of patients with ARDS and control subjects. We measured the copy numbers of 16S rRNA and the serum and BALF cytokines (interleukin [IL]-6, IL-8, receptor for advanced glycation end products, and angiopoietin-2).
RESULTS: We analyzed 47 mechanically ventilated patients diagnosed with (n=40) or without (n=7; control) ARDS. The alpha diversity was significantly decreased in ARDS patients compared with that of the controls (6.24 vs. 8.07, P=0.03). The 16S rRNA gene copy numbers were increased in the ARDS group compared with the controls (3.83 × 106 vs. 1.01 × 105 copies/mL, P=0.06). ARDS patients were subdivided into the hospital survivor (n=24) and non-survivor groups (n=16). Serum IL-6 levels were significantly higher in the non-survivors than in the survivors (567 vs. 214 pg/mL, P=0.027). The 16S rRNA copy number was significantly correlated with serum IL-6 levels in non-survivors (r=0.615, P<0.05). The copy numbers and relative abundance of betaproteobacteria were significantly lower in the non-survivors than in the survivors (713 vs. 7812, P=0.012; 1.22% vs. 0.08%, P=0.02, respectively). Conversely, the copy numbers of Staphylococcus, Streptococcus and Enterobacteriaceae were significantly correlated with serum IL-6 levels in the non-survivors (r=0.579, P<0.05; r=0.604, P<0.05; r=0.588, P<0.05, respectively).
CONCLUSION: The lung bacterial burden was increased, and the alpha diversity was significantly decreased in ARDS patients. The decreased Betaproteobacteria and increased Staphylococcus, Streptococcus and Enterobacteriaceae represented a unique microbial community structure that was correlated with increased serum IL-6 and hospital mortality.

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