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Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression
Published on: June 15, 2019
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CD39 improves survival in microbial sepsis by attenuating systemic inflammation
Balázs Csóka1, Zoltán H Németh2, Gábor Törő
1Department of Surgery and Center for Immunity and Inflammation, Rutgers New Jersey Medical School, Newark, New Jersey, USA;
Summary
Ectonucleoside triphosphate diphosphohydrolase 1 (CD39) protects against sepsis by reducing inflammation and organ damage. Upregulating CD39 may offer a novel therapeutic strategy for sepsis treatment.
Area of Science:
- Immunology
- Biochemistry
- Critical Care Medicine
Background:
- Sepsis is a leading cause of death in critically ill patients, driven by excessive inflammation and organ failure.
- Ectonucleoside triphosphate diphosphohydrolase 1 (CD39) metabolizes extracellular ATP/ADP, regulating purinergic signaling, but its role in sepsis is unexplored.
Purpose of the Study:
- To investigate the role of CD39 in regulating the host response to sepsis.
- To determine if CD39 modulates inflammation, organ damage, and mortality during sepsis.
Main Methods:
- Utilized mouse models of polymicrobial sepsis induced by cecal ligation and puncture.
- Employed CD39 knockout mice, pharmacologic blockade with sodium polyoxotungstate, and bone marrow chimeric mice.
- Assessed mortality, inflammation, organ damage, immune cell apoptosis, and bacterial load.
Main Results:
- CD39 activity (apyrase mimic) reduced sepsis mortality, while CD39 knockout or blockade increased mortality.
- CD39 expression attenuated inflammation, organ damage, immune cell apoptosis, and bacterial load.
- CD39 expression on myeloid cells was critical for reducing inflammation; it was upregulated in sepsis and by E. coli stimulation.
Conclusions:
- CD39 acts as an inducible, evolutionarily conserved protective pathway during sepsis.
- CD39 expression, particularly on myeloid cells, mitigates sepsis-induced organ damage and mortality.
- CD39 represents a promising novel therapeutic target for managing sepsis.
