Journal
CELLS
Volume 10, Issue 2, Pages -Publisher
MDPI
DOI: 10.3390/cells10020384
Keywords
neutrophil extracellular traps; neutrophils; platelets; systemic inflammation; sepsis; endotoxemia; obesity
Categories
Funding
- National Science Center, Poland [2014/15/B/NZ6/02519]
- BioS Priority Research Area under the program Excellence Initiative - Research University at the Jagiellonian University in Krakow
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Obese individuals have a higher survival rate during sepsis, but their white blood cell response in liver vasculature is suppressed; the study found that platelets in obese mice have a limited impact on neutrophil formation, suggesting that their dysfunctional state may affect immune responses.
Systemic inflammation is a detrimental condition associated with high mortality. However, obese individuals seem to have higher chances of surviving sepsis. To elucidate what immunological differences exist between obese and lean individuals we studied the course of endotoxemia in mice fed high-fat diet (HFD) and ob/ob animals. Intravital microscopy revealed that neutrophil extracellular trap (NET) formation in liver vasculature is negligible in obese mice in sharp contrast to their lean counterparts (ND). Unlike in lean individuals, neutrophil influx is not driven by leptin or interleukin 33 (IL-33), nor occurs via a chemokine receptor CXCR2. In obese mice less platelets interact with neutrophils forming less aggregates. Platelets transfer from ND to HFD mice partially restores NET formation, and even further so upon P-selectin blockage on them. The study reveals that in obesity the overexaggerated inflammation and NET formation are limited during sepsis due to dysfunctional platelets suggesting their targeting as a therapeutic tool in systemic inflammation.
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