FPR1 signaling aberrantly regulates S100A8/A9 production by CD14⁺FCN1^hi macrophages and aggravates pulmonary pathology in severe COVID-19.

ABSTRACT: Excessive alarmins S100A8/A9 escalate the inflammation and even exacerbate immune-driven thrombosis and multi-organ damage. However, the regulatory mechanisms of S100A8/A9 expression in infectious diseases remain unclear. In this study, high-dimensional transcriptomic data analyses revealed a high proportion of CD14⁺FCN1^hi macrophages within the pulmonary niche post-severe SARS-CoV-2 infection. By constructing the S100-coexpression gene list and supervised module scoring, we found that CD14⁺FCN1^hi macrophages presented the highest scores of alarmin S100, and possibly served as the trigger and amplifier of inflammation in severe COVID-19. These CD14⁺FCN1^hi cells lacked the positive regulatory activity of transcription factor

SUBMITTER: Wang Z 

PROVIDER: S-EPMC11473795 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature