Hyperinflammatory environment drives dysfunctional myeloid cell effector response to bacterial challenge in COVID-19
Research Article
[키워드] abrogated
Anti-inflammatory therapy
anti-inflammatory treatment
autocrine
Bacterial
Bacterial infection
bacterial superinfection
bacterial superinfections
caused
CD11b
CD163
CD66b
CD86
Cell
cellular
characterized
classical
Clusters
complicate
Course
COVID-19
COVID-19 patient
COVID-19 patients
Critically ill
CRP
CXCR1
CXCR2
CXCR4
cytokine
cytokine levels
cytokine signaling
Dexamethasone
disease severity
driven by
dysregulated
dysregulation
elevated
Ex vivo
exacerbate
exhibited
expression
function
functional
HLA-DR
host response
host-response
hypercytokinemia
Hyperinflammatory
ICU
IFN-γ
IL-4
IL-6 level
Immune cell
immune cells
immune response
IMPROVE
increased mortality
induce
Inflammatory marker
inflammatory mediator
Inflammatory mediators
innate immune function
Innate immunity
low expression
monocyte
Monocytes
MPO
myeloid cell
NET
neutrophil
paracrine
paralysis
patients
phenotype
phenotypic
plasma
provide
receiving
reduced
reduction
reduction in
reflected
response
ROS production
SARS-CoV-2
SARS-CoV-2 pathogenesis
subsequent
suppressed
surface receptor
Symptom
synergistic
systemic inflammation
the disease
TNF-α
treated
utility
[DOI] 10.1371/journal.ppat.1010176 PMC 바로가기 [Article Type] Research Article
[DOI] 10.1371/journal.ppat.1010176 PMC 바로가기 [Article Type] Research Article