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. 2022 Jun 30:15:3437-3445.
doi: 10.2147/IDR.S368772. eCollection 2022.

Expression of Serum Cytokines Profile in Neonatal Sepsis

Suipeng Chen #  1 , Mengjiao Kuang #  1 , Ying Qu  1   2 , Shirui Huang  1 , Binbin Gong  1 , Suzhen Lin  1 , Huiyan Wang  1 , Guiye Wang  1 , Hongqun Tao  1 , Jian Yu  1 , Zuqin Yang  3 , Minghua Jiang  1 , Qipeng Xie  1
Affiliations

Expression of Serum Cytokines Profile in Neonatal Sepsis

Suipeng Chen et al. Infect Drug Resist. .

Abstract

Objective: Sepsis remains a major cause of neonatal death. To better characterize the inflammatory response during neonatal sepsis, we compared the differences in serum cytokines and chemokines between full-term neonates with sepsis and without infection.

Methods: We enrolled 40 full-term neonates with sepsis and 26 full-term neonates without infection as controls between October 2016 and June 2018. Forty cytokines /chemokines in serum were analyzed using the Luminex Bead Immunoassay System.

Results: Our results showed that serum IL-6, IL-8, TNF-α, IL-1β, MIF, CXCL13, CXCL1, CXCL2, CXCL5, CXCL6, CXCL16, CCL27, CCL2, CCL8, CCL3, CCL20, CCL23, and CX3CL1 levels were significantly increased in neonates with sepsis compared to those in the control group (all p<0.05). The levels of serum CCL20, and IL-17 were higher in late-onset sepsis (LOS) than those in early-onset sepsis (EOS) (all p<0.05). Conversely, serum CXCL16 was lower in LOS than that in EOS (p<0.05).

Conclusion: Our findings revealed that excessive pro-inflammatory cytokines might be involved in neonatal sepsis. In addition, chemokines significantly increased the recruitment of immune cells after infection to participate in the anti-infection defense of neonates, but this could lead to damage.

Keywords: chemokines; cytokines; neonatal sepsis.

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Conflict of interest statement

The authors report no conflicts of interest in this work.

Figures

Figure 1
Figure 1
The chemokines and cytokines were significantly different between controls and neonatal sepsis. The levels of CXCL13 (A), CCL27 (B), CXCL5 (C), CX3CL1 (D), CXCL6 (E), CXCL1 (F), CXCL2 (G), IL-1β (H), IL-6 (I), IL-8 (J), CCL2 (K), CCL8 (L), MIF (M), CCL3 (N), CCL20 (O), CCL23 (P), TNF-α (Q), and CXCL16 (R) in serum from controls (n=26) and neonatal sepsis (n=40). The red horizontal lines show the medians and interquartile range. The difference between control and neonatal sepsis was assessed using the Mann–Whitney U-test.
Figure 2
Figure 2
The levels of IL-17 (A), CCL20 (B), and IL-16 (C) in serum from control(n=26, EOS (n=10) and LOS (n=30). The red horizontal lines show the medians and interquartile range. The difference between control and neonatal sepsis was assessed using the Kruskal–Wallis H-test. *P < 0.05; **P < 0. 01.
Figure 3
Figure 3
Levels of cytokines and chemokines before and after treatment in 15 neonates with sepsis. The levels of CXCL13 (A), CX3CL1 (B), IL-1β (C), IL-6 (D), IL-8 (E), IL-16 (F), MIF (G), CCL23 (H), CXCL16 (I), and TNF-alpha (J) in serum from sepsis neonates (n=15) before and after treatment. Differences before and after treatment were analyzed using the Wilcoxon test.
See this image and copyright information in PMC

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