Abstract
Objective Immune dysfunction, including prominent apoptosis of immune cells and decreased functioning of the remaining immune cells, plays a central role in the pathogenesis of sepsis. Sterile α and HEAT/armadillo motif-containing protein (SARM) is implicated in the regulation of immune cell apoptosis. This study aimed to elucidate SARM contributes to sepsis-induced immune cell death and immunosuppression. Methods A mouse model of polymicrobial sepsis was generated by cecum ligation and puncture (CLP). SARM gene and protein expression, caspase 3 cleavage and intracellular ATP production were measured in the mouse spleens. Results CLP-induced polymicrobial sepsis specifically attenuated both the gene and protein expression of SARM in the spleens. Moreover, the attenuation of SARM expression synchronized with splenocyte apoptosis, as evidenced by increased caspase 3 cleavage and ATP depletion. Conclusions These findings suggest that SARM is a potential regulator of sepsis-induced splenocyte apoptosis.
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Acknowledgments
This work was supported financially by Guangzhou Medical University (2011C43), the Third Affiliated Hospital of Guangzhou Medical University (2012Y20), and Department of Education of Guangdong Province (2015KQNCX137).
Author Contributions
Y.G. designed and did experiments, analyzed data, and wrote the manuscript. L.Z. and DZ.C. helped with the experiments. W.C. and DJ.C.contributed reagents and suggestions.
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All of the animal care and procedures were performed according to the protocols approved by the Animal Experimental Committee of Guangzhou Medical University or the Subcommittee on Research Animal Care of Massachusetts General Hospital and were in accordance with the Guangdong Animal Center guidelines for the ethical treatment of animals or the “Guide for the Care and Use of Laboratory Animals” published by the National Institutes of Health.
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Gong, Y., Zou, L., Cen, D. et al. Reduced Expression of SARM in Mouse Spleen during Polymicrobial Sepsis. Inflammation 39, 1930–1938 (2016). https://doi.org/10.1007/s10753-016-0428-x
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DOI: https://doi.org/10.1007/s10753-016-0428-x