An article published this year in “JOURNAL OF IMMUNOLOGY” using our allophycocyanin-conjugated anti-human CD14, PE-conjugated anti-human CD16 (B73.1) and FITC-conjugated anti–HLA-DR, by our customers
from Tumor Immunology Laboratory, Hospital La Paz Institute for Health
Research, La Paz University Hospital, Madrid, Spain, in the study of how
Circulating Monocytes Exhibit an Endotoxin Tolerance Status after Acute
Ischemic Stroke: Mitochondrial DNA as a Putative Explanation for Poststroke
Infections. Congrats and Thanks.
Summary:
Patients with acute ischemic
stroke (AIS) suffer from infections associated with mortality. The relevance of
the innate immune system, and monocytes in particular, has emerged as an
important factor in the evolution of these infections. The study enrolled 14
patients with AIS, without previous treatment, and 10 healthy controls. In the
present study, we show that monocytes from patients with AIS exhibit a
refractory state or endotoxin tolerance. The patients were unable to
orchestrate an inflammatory response against LPS and expressed three factors reported
to control the evolution of human monocytes into a refractory state:
IL-1R–associated kinase-M, NFkB2/p100, and hypoxia-inducible factor-1α. The
levels of circulating mitochondrial DNA (mtDNA) in patients with AIS correlated
with impaired inflammatory response of isolated monocytes. Interestingly, the
patients could be classified into two groups: those who were infected and those
who were not, according to circulating mtDNA levels. This finding was validated
in an independent cohort of 23 patients with AIS. Additionally, monocytes from
healthy controls, cultured in the presence of both sera from patients and
mtDNA, reproduced a refractory state after endotoxin challenge. This effect was
negated by either a TLR9 antagonist or DNase treatment. The present data
further extend our understanding of endotoxin tolerance implications in AIS. A
putative role of mtDNA as a new biomarker of stroke-associated infections, and
thus a clinical target for preventing poststroke infection, has also been
identified.
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