MiR-185-5p measurement assists in reflecting Th1/Th2 cell imbalance, inflammatory cytokine production, and exacerbation risk for childhood asthma

• Chunmei Li ^[1] ; Yiran Zhao ^[1] ; Chunquan Cai ^[2] ; Zhenkui Liu ^[3] ; Junshuai Ma ^[3] ; Yanhong Song ^[3] ; Yanwen Zhang ^[3] ; Weiping Guo ^[3] ; Yanhui Lu ^[3] ; Jing Xing ^[3] ; Yanfei Wang ^[3] ; Wenbin Li ^[3] ; Wei Shi ^[3] ; Haixin Qu ^[3]
  1. [1] Tianjin Medical University

     Tianjin Medical University

     China

     
  2. [2] Department of Neurosurgery, Tianjin Institute of Pediatrics, Tianjin Children's Hospital, Tianjin, China.
  3. [3] Department of Pediatric, The First Affiliated Hospital of Hebei North University, Zhangjiakou, China.

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• Localización: Allergologia et immunopathologia: International journal for clinical and investigate allergology and clinical immunology, ISSN-e 1578-1267, ISSN 0301-0546, Vol. 51, Nº. 3, 2023, págs. 91-98
• Idioma: inglés
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• Resumen

  • Background: MicroRNA (miR)-185-5p participates in the pathology of asthma by regulating immune imbalance, inflammation, periostin synthesis, and smooth muscle contraction. This study intended to explore the dysregulation of miR-185p and its correlation with T-helper (Th)1, Th2 cells, and inflammatory cytokines in childhood asthma.

    Methods: In 150 childhood asthma patients and 30 healthy controls (HCs), miR-185-5p from peripheral blood mononuclear cells was detected using reverse transcription-quantitative polymerase chain reaction, Th cells from peripheral blood samples were detected using flow cytometry, inflammatory cytokines from serum samples were detected using enzyme-linked immunosorbent assay.

    Results: MiR-185-5p was increased in childhood asthma patients versus HCs [median (interquartile range (IQR)): 2.315 (1.770–3.855) versus 1.005 (0.655–1.520)] (P < 0.001). Meanwhile, miR-185-5p was negatively associated with Th1 cells (P = 0.035) but positively correlated with Th2 cells (P = 0.006) and IL-4 (P = 0.003) in childhood asthma patients; however, miR-185-5p was not linked to Th1 cells, Th2 cells, IFN-γ, or IL-4 in HCs (all P > 0.05). In addition, miR-185-5p was positively related to TNF-α (P < 0.001), IL-1β (P = 0.015), and IL-6 (P = 0.008) in childhood asthma patients, miR-185-5p was only linked to TNF-α (P = 0.040) but not IL-1β or IL-6 (both P > 0.05) in HCs. Moreover, miR-185-5p was increased in exacerbated childhood asthma patients versus remissive patients [median (IQR): 3.170 (2.070–4.905) versus 1.900 (1.525–2.615)] (P < 0.001). Besides, miR-185-5p was highest in patients with severe exacerbation followed by patients with moderate exacerbation, and lowest in patients with mild exacerbation (P = 0.010).

    Conclusion: MiR-185-5p is associated with imbalanced Th1/Th2 cells, increased inflammatory cytokines along with elevated exacerbation risk, and severity in childhood asthma patients.