TY - JOUR
T1 - Specificity of Presepsin as a Biomarker of Bacterial Infection in Mouse Sepsis Models
AU - Hosokawa, Kyosuke
AU - Obara, Hideaki
AU - Fukuda, Kazumasa
AU - Mastubara, Kentaro
AU - Kitagawa, Yuko
N1 - Funding Information:
H.O. has received grant from LSI Medience Corporation (Tokyo, Japan).
Publisher Copyright:
© 2022 Elsevier Inc.
PY - 2023/3
Y1 - 2023/3
N2 - Introduction: Since its discovery in 2002, presepsin (P-SEP) has been reported to be useful in the early diagnosis of sepsis and has been evaluated in many clinical studies. However, as antibodies that bind to mouse P-SEP were previously unavailable, serum P-SEP levels in mice are limited. This study used a P-SEP enzyme-linked immunosorbent assay kit to evaluate the changes in serum P-SEP levels in mouse sepsis models compared with changes in other inflammatory markers and determine whether P-SEP can function as a biomarker specific to bacterial infections. Methods: Sepsis was induced in mice via cecal ligation and puncture (CLP), induction with lipopolysaccharide (LPS), and cecal ligation (CL) model was created as a control for the CLP model, following which clinical biomarkers (P-SEP, C-reactive protein, and procalcitonin) were evaluated. Results: The 48-h survival rates in the CLP, CL, and LPS-induced sepsis models were 67%, 89%, and 57%, respectively. Serum C-reactive protein levels did not increase in the CLP and CL models within 24 h but significantly increased in the LPS-induced sepsis model. Serum procalcitonin levels increased in the CLP and CL models and especially increased in the LPS-induced sepsis model. In contrast, an increase in serum P-SEP level was found in the CLP model at 6 h compared with those at baseline, the CL, and LPS-induced sepsis models. Conclusions: Mouse P-SEP is elevated early in infection and more specific to bacterial infection compared with other biomarkers.
AB - Introduction: Since its discovery in 2002, presepsin (P-SEP) has been reported to be useful in the early diagnosis of sepsis and has been evaluated in many clinical studies. However, as antibodies that bind to mouse P-SEP were previously unavailable, serum P-SEP levels in mice are limited. This study used a P-SEP enzyme-linked immunosorbent assay kit to evaluate the changes in serum P-SEP levels in mouse sepsis models compared with changes in other inflammatory markers and determine whether P-SEP can function as a biomarker specific to bacterial infections. Methods: Sepsis was induced in mice via cecal ligation and puncture (CLP), induction with lipopolysaccharide (LPS), and cecal ligation (CL) model was created as a control for the CLP model, following which clinical biomarkers (P-SEP, C-reactive protein, and procalcitonin) were evaluated. Results: The 48-h survival rates in the CLP, CL, and LPS-induced sepsis models were 67%, 89%, and 57%, respectively. Serum C-reactive protein levels did not increase in the CLP and CL models within 24 h but significantly increased in the LPS-induced sepsis model. Serum procalcitonin levels increased in the CLP and CL models and especially increased in the LPS-induced sepsis model. In contrast, an increase in serum P-SEP level was found in the CLP model at 6 h compared with those at baseline, the CL, and LPS-induced sepsis models. Conclusions: Mouse P-SEP is elevated early in infection and more specific to bacterial infection compared with other biomarkers.
KW - C-Reactive protein
KW - Cecal ligation and puncture
KW - Lipopolysaccharide
KW - Presepsin
KW - Procalcitonin
KW - Sepsis
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U2 - 10.1016/j.jss.2022.10.063
DO - 10.1016/j.jss.2022.10.063
M3 - Article
C2 - 36442256
AN - SCOPUS:85142760021
SN - 0022-4804
VL - 283
SP - 572
EP - 580
JO - Journal of Surgical Research
JF - Journal of Surgical Research
ER -