[Serum levels of interleukin-38 and interleukin-1β in the acute phase of Kawasaki disease in children]

Zhongguo Dang Dai Er Ke Za Zhi. 2018 Jul;20(7):543-548. doi: 10.7499/j.issn.1008-8830.2018.07.006.
[Article in Chinese]

Abstract

Objective: To study the expression of serum cytokines, interleukin-38 (IL-38) and interleukin-1β (IL-1β) in the acute phase of Kawasaki disease (KD) in children and the association of IL-38 and IL-1β with inflammatory response in the acute phase and the development of coronary artery lesion (CAL).

Methods: A total of 40 children with KD who were hospitalized in the hospital between July 2015 and June 2016 were enrolled, with 21 children in the CAL group and 19 in the non-CAL (NCAL) group. Thirty healthy children and 19 children with infection and pyrexia, who were matched for sex and age, were enrolled as healthy control group and pyrexia control group respectively. ELISA was used to measure the serum levels of IL-38 and IL-1β in the 40 children in the acute phase of KD. Spearman's rank correlation analysis was used to investigate the correlations of IL-1β and IL-38 with interleukin-6 (IL-6), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), procalcitonin (PCT), N-terminal pro-brain natriuretic peptide (NT-proBNP), triglyceride (TG), and total cholesterol (TC).

Results: The serum level of IL-38 in the children in the acute phase of KD was significantly lower than that in the healthy control group (P<0.05), but significantly higher than that in the pyrexia control group (P<0.05). There was no significant difference in the level of IL-38 between the CAL and NCAL groups (P>0.05). The children in the acute phase of KD had a significantly higher level of IL-1β than the healthy control group (P<0.05), while there was no significant difference between this group and the pyrexia control group (P>0.05). There was also no significant difference in the level of IL-1β between the CAL and NCAL groups (P>0.05). Serum IL-1β and IL-38 levels were not correlated with serum levels of CRP, ESR, PCT, IL-6, and NT-ProBNP or blood lipids (TG and TC) (P>0.05).

Conclusions: IL-38 is involved in an inflammatory response in the acute phase of KD and may exert an anti-inflammatory effect, which is opposite to the effect of IL-1β to promote inflammatory response. However, there is no significant correlation between these two cytokines and the development of CAL in KD.

目的: 通过检测川崎病(KD)患儿急性期血清细胞因子IL-38和IL-1β表达水平,分析IL-38和IL-1β与KD急性期炎症反应以及冠状动脉损伤的相关性,并进一步探讨其临床意义。

方法: 选取2015年7月至2016年6月住院的KD患儿40例为研究对象,其中冠状动脉损伤(CAL)组21例,非冠状动脉损伤(NCAL)组19例;另外选取性别、年龄相匹配的30例健康儿童和19例感染发热患儿作为健康对照组和发热对照组。采用酶联免疫吸附法(ELISA)检测40例川崎病(KD)患儿急性期血清细胞因子IL-38和IL-1β水平。采用Spearman秩相关分析IL-1β和IL-38分别与白细胞介素-6(IL-6)、C-反应蛋白(CRP)、血沉(ESR)、降钙素原(PCT)、氨基末端脑钠肽前体(NT-ProBNP)、甘油三酯(TG)和血总胆固醇(TC)的相关性。

结果: KD患儿急性期血清IL-38水平明显低于健康对照组,但高于发热对照组(P < 0.05);CAL组和NCAL组IL-38水平比较差异无统计学意义(P > 0.05)。KD患儿急性期IL-1β水平较健康对照组明显升高(P < 0.05),但与发热照对组相比差异无统计学意义(P > 0.05);CAL组和NCAL组IL-1β水平比较差异无统计学意义(P > 0.05)。未发现细胞因子IL-1β和IL-38与其他炎性指标(CRP、ESR、PCT、IL-6、NT-ProBNP)及血脂(TG、TC)之间存在相关性(P > 0.05)。

结论: 细胞因子IL-38参与KD急性期炎症反应且可能发挥与IL-1β促进炎症反应相反的抗炎作用,二者与KD伴冠状动脉损伤发生均无明显相关性。

MeSH terms

  • Acute Disease
  • Atrial Natriuretic Factor / blood
  • Blood Sedimentation
  • C-Reactive Protein / metabolism
  • Case-Control Studies
  • Child
  • Child, Preschool
  • Cholesterol / blood
  • Coronary Artery Disease / blood
  • Coronary Artery Disease / etiology
  • Coronary Artery Disease / pathology
  • Coronary Vessels / pathology
  • Female
  • Humans
  • Infant
  • Interleukin-1beta / blood*
  • Interleukins / blood*
  • Male
  • Mucocutaneous Lymph Node Syndrome / blood*
  • Mucocutaneous Lymph Node Syndrome / complications
  • Procalcitonin / blood
  • Protein Precursors / blood
  • Triglycerides / blood

Substances

  • IL-38 protein, human
  • Interleukin-1beta
  • Interleukins
  • N-terminal proatrial natriuretic peptide
  • Procalcitonin
  • Protein Precursors
  • Triglycerides
  • Atrial Natriuretic Factor
  • C-Reactive Protein
  • Cholesterol

Grants and funding

国家自然科学基金(81270949);湖北省卫计委科技项目(WJ2017M057)