Primate Monocytes - CD14, CD16 - Ziegler-Heitbrock


TREM2+ and interstitial-like macrophages orchestrate airway inflammation in SARS-CoV-2 infection in rhesus macaques.


The immunopathological mechanisms driving the development of severe COVID-19 remain poorly defined. Here, we utilize a rhesus macaque model of acute SARS-CoV-2 infection to delineate perturbations in the innate immune system. SARS-CoV-2 initiates a rapid infiltration of plasmacytoid dendritic cells into the lower airway, commensurate with IFNA production, natural killer cell activation, and a significant increase of blood CD14-CD16+ monocytes. To dissect the contribution of lung myeloid subsets to airway inflammation, we generate a longitudinal scRNA-Seq dataset of airway cells, and map these subsets to corresponding populations in the human lung. SARS-CoV-2 infection elicits a rapid recruitment of two macrophage subsets: CD163+MRC1-, and TREM2+ populations that are the predominant source of inflammatory cytokines. Treatment with baricitinib (Olumiant ), a JAK1/2 inhibitor is effective in eliminating the influx of non-alveolar macrophages, with a reduction of inflammatory cytokines. This study delineates the major lung macrophage subsets driving airway inflammation during SARS-CoV-2 infection.

Authors: Upadhyay AA, Viox EG, Hoang TN, Boddapati AK, Pino M, Lee MY, Corry J, Strongin Z, Cowan DA, Beagle EN, Horton TR, Hamilton S, Aoued H, Harper JL, Edwards CT, Nguyen K, Pellegrini KL, Tharp GK, Piantadosi A, Levit RD, Amara RR, Barratt-Boyes SM, Ribeiro S
Journal: Nat Commun;2023Apr06; 14 (1) 1914. doi:10.1038/s41467-023-37425-9
Year: 2023
PubMed: PMID: 37024448 (Go to PubMed)