重症支原体肺炎患儿铁死亡水平与炎症反应、氧化应激的相关性及意义

郑艳兰 ,  谢姣 ,  卢美娟

中国妇幼健康研究 ›› 2024, Vol. 35 ›› Issue (7) : 32 -37.

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中国妇幼健康研究 ›› 2024, Vol. 35 ›› Issue (7) : 32 -37. DOI: 10.3969/j.issn.1673-5293.2024.07.005
专题研究

重症支原体肺炎患儿铁死亡水平与炎症反应、氧化应激的相关性及意义

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Correlations of serum ferroptosis level with inflammatory response and oxidative stress in children with severe Mycoplasma pneumonia and their significance

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摘要

目的 研究重症支原体肺炎(MPP)患儿铁死亡水平与炎症反应、氧化应激的相关性及意义。方法 选择2019年6月至2022年6月我院儿科收治的74例轻症MPP患儿和136重症MPP患儿,分别作为轻症MPP组和重症MPP组,另选择80例健康儿童作为对照组.采集血清并检测铁死亡标志物转铁蛋白受体1(TfR1)、酰基辅酶A合成酶长链家族成员4(ACSL4)、谷胱甘肽过氧化物酶4(GPX4)、炎症反应标志物C反应蛋白(CRP)、白介素-6(IL-6),氧化应激标志物丙二醛(MDA)、过氧化脂质(LPO)的水平,比较三组间各个指标的差异,并分析铁死亡标志物与炎症反应标志物、氧化应激标志物的相关性.评估血清铁死亡标志物诊断重症MPP、预测重症MPP预后的价值。结果 重症MPP组的血清TfR1、ACSL4、CRP、IL-6、MDA、LPO含量高于轻症MPP组和对照组,GPX4含量低于轻症MPP组和对照组(F值为321.061、233.544、839.887、761.429、897.668、585.581和196.558,P<0.05);重症MPP组的血清TfR1、ACSL4与CRP、IL-6、MDA、LPO呈正相关(r值介于0.311至0.441之间,P<0.05),GPX4与CRP、IL-6、MDA、LPO呈负相关(r值介于-0.413至-0.309之间,P<0.05);重症MPP组中预后不良患儿的血清TfR1、ACSL4含量显著高于预后良好患儿,GPX4含量低于存活患儿(t值为5.025、4.535和5.440,P<0.05);血清TfR1、ACSL4、GPX4三项指标联合对重症MPP诊断及预后预测价值最大(AUC=0.973,灵敏度为95.59%,特异度为100%;AUC=0.952,灵敏度为86.96%,特异度为88.46%)。结论 重症MPP患儿铁死亡激活与炎症反应、氧化应激加重相关,血清铁死亡标志物是诊断重症MPP、预测预后的标志物.

Abstract

Objective To study correlations of serum level of ferroptosis with inflammatory response and oxidative stress in children with severe Mycoplasma pneumonia (MPP) and their significance. Methods 74 children with mild MPP and 136 children with severe MPP who admitted to our Department of Pediatrics from June 2019 to June 2022 were selected as the mild MPP group and the severe MPP group respectively, and 80 healthy children were selected as the control group. Serum samples were taken and the serum levels of ferroptosis markers as transferrin receptor 1 (TfR1), Acyl-CoA synthase long chain family member 4 (ACSL4) and glutathione peroxidase 4 (GPX4), inflammatory response markers as C-reactive protein (CRP) and interleukin-6 (IL-6), oxidative stress markers as malondialdehyde (MDA), and lipid peroxide (LPO) were detected, and the differences in serum levels of these indexes among the three groups were compared. The correlations of ferroptosis markers with inflammatory response markers and oxidative stress markers were analyzed. The short-term prognosis of the children with severe MPP was evaluated, and the values of serum ferroptosis markers in diagnosing and predicting prognosis of severe MPP were analyzed. Results The serum levels of TfR1, ACSL4, CRP, IL-6, MDA, and LPO of the children in the severe MPP group were higher than those in the mild MPP group and the control group, while the serum level of GPX4 was lower than that in the mild MPP group and the control group (F=321.061, 233.544, 839.887, 761.429, 897.668, 585.581 and 196.558 respectively, all P<0.05). In the severe MPP group, the serum levels of TfR1 and ACSL4 were positively correlated with the serum levels of CRP, IL-6, MDA and LPO (r=0.311-0.441, all P<0.05), while the serum level of GPX4 was negatively correlated with the serum levels of CRP, IL-6, MDA and LPO (r=-0.413--0.309, all P<0.05). In the severe MPP group, the serum levels of TfR1 and ACSL4 of the children with poor prognoses were higher than those of the children with good prognoses, while the serum level of GPX4 was lower than that of the children with good prognoses (t=5.025, 4.535 and 5.440 respectively, all P<0.05). The combination of serum levels of TfR1, ACSL4 and GPX4 had the highest diagnostic value and predictive value for prognosis of severe MPP (for diagnostic value: AUC=0.973, the sensitivity was 95.59% and the speciality was 100%; for predictive value: AUC=0.952, the sensitivity was 86.96% and the speciality was 88.46%). Conclusion Activation of ferroptosis in children with severe MPP relates with increased inflammation and oxidative stress. Serum ferroptosis markers are indicators for diagnosing severe MPP and predicting the prognosis.

关键词

肺炎支原体肺炎 / 铁死亡 / 炎症反应 / 氧化应激 / 相关性 / 诊断

Key words

Mycoplasma pneumoniae pneumonia / ferroptosis / inflammatory reactions / oxidative stress / correlation / diagnosis

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郑艳兰,谢姣,卢美娟. 重症支原体肺炎患儿铁死亡水平与炎症反应、氧化应激的相关性及意义[J]. 中国妇幼健康研究, 2024, 35(7): 32-37 DOI:10.3969/j.issn.1673-5293.2024.07.005

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参考文献

[1]

Biagi C, Cavallo A, Rocca A, et al. Pulmonary and Extrapulmonary Manifestations in Hospitalized Children with Mycoplasma Pneumoniae Infection[J]. Microorganisms, 2021, 9(12): 2553.

[2]

Desai S, Hall M, Lipsett SC, et al. Mycoplasma Pneumoniae Testing and Treatment Among Children With Community-Acquired Pneumonia[J]. Hospital Pediatrics, 2021, 11(7): 760-763.

[3]

Tang D, Chen X, Kang R, et al. Ferroptosis: molecular mechanisms and health implications[J]. Cell Res, 2021, 31(2): 107-125.

[4]

Li Z, Yu Y, Liu C, et al. Identification of the key ferroptosis-related genes involved in sepsis progression and experimental validation in vivo[J]. Frontiers in Pharmacology, 2022, 13: 940261.

[5]

Xu B, Wang H, Chen Z. Puerarin Inhibits Ferroptosis and Inflammation of Lung Injury Caused by Sepsis in LPS Induced Lung Epithelial Cells[J]. Frontiers in Pediatrics, 2021, 9: 706327.

[6]

赵丽娜, 葛国岚, 李靖, 等. 蛇床子素通过Nrf2-Gpx4铁死亡途径对肺炎支原体肺炎大鼠肺损伤的改善作用[J]. 中成药, 2023, 45(1): 48-54.

[7]

中华医学会儿科学分会呼吸学组, 《中华实用儿科临床杂志》编辑委员会. 儿童肺炎支原体肺炎诊治专家共识(2015年版)[J]. 中华实用儿科临床杂志, 2015, 30(17): 1304-1308.

[8]

Chen L, Yin J, Liu X, et al. Thromboembolic complications of Mycoplasma pneumoniae pneumonia in children[J]. The clinical respiratory journal, 2023, 17(3): 187-196.

[9]

黎念. 儿童重症肺炎支原体肺炎的临床特点及预后[J]. 中国全科医学, 2019, 22(S2): 61-64.

[10]

Xiao L, Huang H, Fan S, et al. Ferroptosis: A mixed blessing for infectious diseases[J]. Frontiers in Pharmacology, 2022, 13: 992734.

[11]

Li Y, Yang Y, Yang Y. Multifaceted Roles of Ferroptosis in Lung Diseases[J]. Frontiers in Molecular Biosciences, 2022, 9: 919187.

[12]

Bagayoko S, Meunier E. Emerging roles of ferroptosis in infectious diseases.[J]. The FEBS journal, 2021, 289(24): 7869-7890.

[13]

Ding H, Chen S, Pan X, et al. Transferrin receptor 1 ablation in satellite cells impedes skeletal muscle regeneration through activation of ferroptosis[J]. Journal of cachexia, sarcopenia and muscle, 2021, 12(3): 746-768.

[14]

Yu S, Li Z, Zhang Q, et al. GPX4 degradation via chaperone-mediated autophagy contributes to antimony-triggered neuronal ferroptosis.[J]. Ecotoxicology and environmental safety, 2022, 234: 113413.

[15]

Liu L, Kang X. ACSL4 is overexpressed in psoriasis and enhances inflammatory responses by activating ferroptosis[J]. Biochemical and Biophysical Research Communications, 2022, 623: 1-8.

基金资助

衡阳市科学技术局(S2018N9031034365)

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