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[Preprint]. 2021 Nov 30:2021.03.23.21253487. Originally published 2021 Mar 26. [Version 2] doi: 10.1101/2021.03.23.21253487

Impaired immune signaling and changes in the lung microbiome precede secondary bacterial pneumonia in COVID-19

Alexandra Tsitsiklis, Beth Shoshana Zha, Ashley Byrne, Catherine DeVoe, Elze Rackaityte, Sophia Levan, Sara Sunshine, Eran Mick, Rajani Ghale, Christina Love, Alexander J Tarashansky, Angela Pisco, Jack Albright, Alejandra Jauregui, Aartik Sarma, Norma Neff, Paula Hayakawa Serpa, Thomas J Deiss, Amy Kistler, Sidney Carrillo, K Mark Ansel, Aleksandra Leligdowicz, Stephanie Christenson, Angela Detweiler, Norman G Jones, Bing Wu, Spyros Darmanis, Susan V Lynch, Joseph L DeRisi; COMET Consortium, Michael A Matthay, Carolyn M Hendrickson, Kirsten N Kangelaris, Matthew F Krummel, Prescott G Woodruff, David J Erle, Oren Rosenberg, Carolyn S Calfee, Charles R Langelier
PMCID: PMC8010763  PMID: 33791731

Abstract

Secondary bacterial infections, including ventilator-associated pneumonia (VAP), lead to worse clinical outcomes and increased mortality following viral respiratory infections including in patients with coronavirus disease 2019 (COVID-19). Using a combination of tracheal aspirate bulk and single-cell RNA sequencing we assessed lower respiratory tract immune responses and microbiome dynamics in 23 COVID-19 patients, 10 of whom developed VAP, and eight critically ill uninfected controls. At a median of three days (range: 2-4 days) before VAP onset we observed a transcriptional signature of bacterial infection. At a median of 15 days prior to VAP onset (range: 8-38 days), we observed a striking impairment in immune signaling in COVID-19 patients who developed VAP. Longitudinal metatranscriptomic analysis revealed disruption of lung microbiome community composition in patients with VAP, providing a connection between dysregulated immune signaling and outgrowth of opportunistic pathogens. These findings suggest that COVID-19 patients who develop VAP have impaired antibacterial immune defense detectable weeks before secondary infection onset.

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