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Siglec-F+ neutrophils in the spleen induce immunosuppression following acute infection

GSE264139 Mus musculus Expression profiling by high throughput sequencing 9 samples Submitted 2024/04/24 Platform GPL24247
Summary
The mechanisms underlying the increased mortality of secondary infections during the immunosuppressive phase of sepsis remain elusive. We established a mouse model of sepsis-induced immunosuppression followed by secondary infection. Compared to other organs, we observed a significant reduction in pro-inflammatory cytokines in the spleen, accompanied by a marked increase in IL-10 production, primarily by infiltrating neutrophils. Furthermore, we confirmed that these infiltrating neutrophils in the spleen during the immunosuppressive phase of sepsis undergo phenotypic change in the local microenvironment, exhibiting high expression of neutrophil biomarkers such as Siglec-F, Ly6G, and Siglec-E. These neutrophils subsequently produced IL-10 to suppress T lymphocytes. Depletion of neutrophils or specifically targeting Siglec-F leads to a notable improvement in the survival of mice with secondary infections. The identification of Siglec-F+ neutrophils as key regulators of immunosuppression following sepsis represents a novel finding with potential therapeutic implications.
Published in
Siglec-F(+) neutrophils in the spleen induce immunosuppression following acute infection
Liao C, Luo S, Liu X et al. · Theranostics 2024 · PMID 38646647 · doi:10.7150/thno.93812
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Also filed as BioProject PRJNA1101046 and SRA study SRP502085. Searching any of these in the dataset finder brings you back here.

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