临床研究

儿童过敏性紫癜口腔菌群及其代谢产物特征

  • 王晴雯 ,
  • 张淑雅 ,
  • 熊维霖 ,
  • 胡晓磊 ,
  • 李紫薇 ,
  • 郭庆寅
展开
  • 1.河南中医药大学 (郑州 450003 )
    2.河南中医药大学第一附属医院 (郑州 450003 )

收稿日期: 2023-06-19

  网络出版日期: 2024-05-15

基金资助

河南省自然科学基金项目(212300410369);河南省中医学“双一流”创建科学研究专项课题(HSRP-DFCTCM-2023-1-17)

Characteristics of oral flora and its metabolites in children with henoch⁃schonlein purpura

  • Qingwen WANG ,
  • Shuya ZHANG ,
  • Weilin XIONG ,
  • Xiaolei HU ,
  • Ziwei LI ,
  • Qingyin. GUO
Expand
  • *.He′nan University of Chinese Medicine,Zhengzhou 450003,China

Received date: 2023-06-19

  Online published: 2024-05-15

摘要

目的 探讨儿童过敏性紫癜(HSP)的口腔菌群及其代谢产物特征,阐明过敏性紫癜发病的机制。 方法 纳入合格受试者3组,其中HSP组20例,紫癜性肾炎(HSPN)组20例,对照组20例。对各组的唾液进行16S rRNA测序和代谢组学分析,分析差异性菌群与差异性代谢物之间的相关性。 结果 (1)与对照组相比,HSPN组丰富度和多样性差异有统计学意义(P < 0.05),HSP组丰富度和多样性差异无统计学意义(P > 0.05)。与HSP组相比,HSPN组丰富度和多样性显著升高(P < 0.05)。其中属水平上,各组中链球菌占比最高。与对照组相比,HSP组无显著性相关菌属,HSPN组假单胞菌属和副拟杆菌属显著增高(P < 0.05)。与HSP组相比,HSPN组假单胞菌属和副拟杆菌属相对丰度显著升高(P < 0.05)。(2)与对照组相比,HSPN组有12种差异性代谢产物,涉及苯丙氨酸代谢等9种代谢途径;HSP组差异无统计学意义代谢产物,无代谢通路。与HSP组相比,HSPN组有15种差异性代谢产物,涉及苯丙氨酸代谢等9种代谢途径。(3)HSPN组与对照组中假单胞菌属、副拟杆菌属与苯丙氨酸代谢途径产物呈负相关。HSPN组与HSP组中假单胞菌属、副拟杆菌属与苯丙氨酸代谢途径产物呈负相关。口腔中参与苯丙氨酸代谢的代谢产物为2-羟基肉桂酸、苯丙酮酸、N-乙酰基-L-苯丙氨酸。 结论 链球菌属、假单胞菌属、副拟杆菌属可能作为HSPN发病的触发因素之一,苯丙氨酸代谢可能是HSPN的发病过程中的通路之一。相比于HSP患儿,HSPN患儿口腔菌群失调更加明显,代谢产物差异性更强。

本文引用格式

王晴雯 , 张淑雅 , 熊维霖 , 胡晓磊 , 李紫薇 , 郭庆寅 . 儿童过敏性紫癜口腔菌群及其代谢产物特征[J]. 实用医学杂志, 2024 , 40(9) : 1244 -1250 . DOI: 10.3969/j.issn.1006-5725.2024.09.011

Abstract

Objective To study and compare the oral microbiota and metabolites of children with Henoch Schonlein purpura(HSP) to identify specific microbiota and metabolites related to this disease and elucidate the pathogenesis of HSP. Methods Three groups of qualified subjects were included, including 20 in the HSP group, 20 in the HSP nephritis (HSPN) group, and 20 in the control group. Perform high?throughput 16S rRNA sequencing and metabolic profiling of saliva from each group to analyze the correlation between differential microbiota and differential metabolites. Results (1) Compared with the control group, there was a significant difference in richness and diversity in the HSPN group (P < 0.05). At the same time, there was no significant difference in richness and diversity in the HSP group (P > 0.05). Compared with the HSP group, the abundance, and diversity of the HSPN group were significantly increased (P < 0.05). At the genus level, the proportion of Streptococcus in each group is the highest. Compared with the control group, there was no significant correlation between the HSP group and the genus of bacteria. In contrast, the HSPN group showed a significant increase in the genera of Pseudomonas and Parabacteroides (P < 0.05). Compared with the HSP group, the abundance of Pseudomonas and Parabacteroides in the HSPN group was significantly increased (P < 0.05). (2) Compared with the control group, the HSPN group had 12 differential metabolites involving nine metabolic pathways, such as phenylalanine metabolism; There was no significant difference in metabolites and no metabolic pathway in the HSP group. Compared with the HSP group, the HSPN group has 15 differential metabolites involving nine metabolic pathways, such as phenylalanine metabolism. (3) In the HSPN and control groups, Pseudomonas and Parabacteroides negatively correlated with Phenylalanine metabolic pathway products. In the HSPN and HSP groups, Pseudomonas, Parabacteroides, and Phenylalanine metabolic pathway products were negatively correlated. The metabolites involved in phenylalanine metabolism in the oral cavity are 2?hydroxycinnamic acid, Phenylpyruvic acid, and N?acetyl?L?phenylalanine. Conclusion There is a significant difference between HSPN and HSP children and healthy children. Streptococcus, Pseudomonas, and Parabacteroides may be one of the trigger factors of HSPN, and Phenylalanine metabolism may be one of the pathways in the pathogenesis of HSPN. Children with HSPN have a more pronounced imbalance in oral microbiota and greater differences in metabolic products than children with HSP.

参考文献

1 PERUZZI L, COPPO R. IgA vasculitis nephritis in children and adults: one or different entities?[J]. Pediatr Nephrol, 2021,36(9):2615-2625. doi:10.1007/s00467-020-04818-7
2 PILLEBOUT E, SUNDERKOTTER C. IgA vasculitis[J]. Semin Immunopathol, 2021,43(5):729-738. doi:10.1007/s00281-021-00874-9
3 WANG J J, XU Y, LIU F F, et al. Association of the infectious triggers with childhood Henoch-Schonlein purpura in Anhui province, China[J]. J Infect Public Health, 2020,13(1):110-117. doi:10.1016/j.jiph.2019.07.004
4 NOSSENT J C, RAYMOND W, KEEN H, et al. Infection Rates Before and After Diagnosis of IgA Vasculitis in Childhood: A Population-wide Study Using Non-exposed Matched Controls[J]. J Rheumatol, 2020,47(3):424-430. doi:10.3899/jrheum.190110
5 CHEN B, WANG J, WANG Y, et al. Oral microbiota dysbiosis and its association with Henoch-Schonlein Purpura in children[J]. Int Immunopharmacol, 2018,65:295-302. doi:10.1016/j.intimp.2018.10.017
6 PANG S, ZHAO S, BAI X, et al. Variations of tongue coating microbiota in children with Henoch-Schonlein purpura nephritis[J]. Microb Pathog, 2021,160:105192. doi:10.1016/j.micpath.2021.105192
7 吴小川,唐雪梅,胡坚,等. 儿童过敏性紫癜循证诊治建议[J]. 中华儿科杂志, 2013,51(7):502-507.
8 中华医学会儿科学分会肾脏学组. 紫癜性肾炎诊治循证指南(2016)[J]. 中华儿科杂志, 2017,55(9):647-651. doi:10.3760/cma.j.issn.0578-1310.2017.09.003
9 KHOR B, SNOW M, HERRMAN E, et al. Interconnections Between the Oral and Gut Microbiomes: Reversal of Microbial Dysbiosis and the Balance Between Systemic Health and Disease[J]. Microorganisms, 2021, 9(3):496. doi:10.3390/microorganisms9030496
10 KITAMOTO S, NAGAO-KITAMOTO H, HEIN R, et al. The Bacterial Connection between the Oral Cavity and the Gut Diseases[J]. J Dent Res, 2020,99(9):1021-1029. doi:10.1177/0022034520924633
11 KONG X, LIU J, CETINBAS M, et al. New and Preliminary Evidence on Altered Oral and Gut Microbiota in Individuals with Autism Spectrum Disorder (ASD): Implications for ASD Diagnosis and Subtyping Based on Microbial Biomarkers[J]. Nutrients, 2019, 11(9):2128. doi:10.3390/nu11092128
12 IWAUCHI M, HORIGOME A, ISHIKAWA K, et al. Relationship between oral and gut microbiota in elderly people[J]. Immun Inflamm Dis, 2019,7(3):229-236. doi:10.1002/iid3.266
13 WANG X, ZHANG L, WANG Y, et al. Gut microbiota dysbiosis is associated with Henoch-Schonlein Purpura in children[J]. Int Immunopharmacol, 2018,58:1-8. doi:10.1016/j.intimp.2018.03.003
14 ZHOU F, SHAO Q, JIA L, et al. Gut Microbiota Variations between Henoch-Schonlein Purpura and Henoch-Schonlein Purpura Nephritis[J]. Gastroenterol Res Pract, 2022,2022:4003491. doi:10.1155/2022/4003491
15 TAN J, ZHONG Z, TANG Y, et al. Intestinal dysbiosis featuring abundance of Streptococcus associates with Henoch-Schonlein purpura nephritis (IgA vasculitis with nephritis) in adult[J]. BMC Nephrol, 2022,23(1):10. doi:10.1186/s12882-021-02638-x
16 TIKHOMIROVA A, ZILM P S, TRAPPETTI C, et al. The central role of arginine in Haemophilus influenzae survival in a polymicrobial environment with Streptococcus pneumoniae and Moraxella catarrhalis[J]. PLoS One, 2022,17(7):e271912. doi:10.1371/journal.pone.0271912
17 MARTINEZ R, HERRERA J, PEREZ R, et al. Frequency of Porphyromonas gingivalis and fimA genotypes in patients with periodontitis and systemic lupus erythematosus[J]. Lupus, 2021,30(1):80-85. doi:10.1177/0961203320969983
18 BHANDARI S, BISHT K S, MERKLER D J. The Biosynthesis and Metabolism of the N-Acylated Aromatic Amino Acids: N-Acylphenylalanine, N-Acyltyrosine, N-Acyltryptophan, and N-Acylhistidine[J]. Front Mol Biosci, 2021,8:801749. doi:10.3389/fmolb.2021.801749
19 ROSA A P, JACQUES C E, MORAES T B, et al. Phenylpyruvic acid decreases glucose-6-phosphate dehydrogenase activity in rat brain[J]. Cell Mol Neurobiol, 2012,32(7):1113-1118. doi:10.1007/s10571-012-9834-2
文章导航

/