miR-142-3p alleviates house dust mite-induced airway inflammation among children

WU Feng; SONG Tingting; ZANG Xiao; HONG Shanchao; WANG Wei

doi:10.16835/j.cnki.1000-9817.2023.12.026

Volume 44 Issue 12

Dec. 2023

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WU Feng, SONG Tingting, ZANG Xiao, HONG Shanchao, WANG Wei. miR-142-3p alleviates house dust mite-induced airway inflammation among children[J]. CHINESE JOURNAL OF SCHOOL HEALTH, 2023, 44(12): 1883-1888. doi: 10.16835/j.cnki.1000-9817.2023.12.026

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WU Feng, SONG Tingting, ZANG Xiao, HONG Shanchao, WANG Wei. miR-142-3p alleviates house dust mite-induced airway inflammation among children[J]. CHINESE JOURNAL OF SCHOOL HEALTH, 2023, 44(12): 1883-1888. doi: 10.16835/j.cnki.1000-9817.2023.12.026

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miR-142-3p alleviates house dust mite-induced airway inflammation among children

doi: 10.16835/j.cnki.1000-9817.2023.12.026

WU Feng¹,
SONG Tingting¹,
ZANG Xiao²,
HONG Shanchao^{1
,
,},
WANG Wei^{3
,
,}

1.
Department of Clinical Laboratory, Jiangnan University Medical Center, Wuxi (214001), Jiangsu Province, China

Received Date: 2023-09-26
Rev Recd Date: 2023-10-18

Available Online: 2023-12-26

Publish Date: 2023-12-25

Abstract

Abstract

Objective To investigate the role of miR-142-3p in alleviation of house dust mite-induced allergic airway inflammation among children, so as to provide insights into unraveling the pathogenesis of allergic airway inflammation. Methods Serum samples were collected from 15 patients with house dust mite-induced allergic asthma and 15 healthy children in Jiangnan University Medical Center from September to November 2022, and serum miR-142-3p expression was quantified using a fluorescent quantitative real-time PCR (qPCR) assay. The levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were measured in the cell culture supernatant using enzyme-linked immunosorbent assay (ELISA), and the expression of high mobility group box 1 (HMGB1) was detected at transcriptional and translational lvels using qPCR and Western blotting assays. The negative regulation of the HMGB1 gene by miR-142-3p was identified using a dual luciferase gene reporter assay, and the expression of downstream regulatory proteins was determined in human normal lung epithelial cells (BEAS-2B) cells transfected with miR-142-3p using Western blotting. In addition, female C57BL/6 mice at ages of 6-8 weeks were randomly assigned to the phosphate buffer saline (PBS) group, house dust mite-sensitized airway inflammation group and house dust mite-sensitized airway inflammation + miR-142-3p intervention group. Mouse airway inflammation was evaluated using hematoxylin-eosin staining, and the expression of inflammatory cells and inflammatory cytokines were detected in mouse bronchoalveolar lavage fluid (BALF) using Giemsa staining and ELISA. Results Lower serum miR-142-3p expression was quantified among children with house dust mite-induced allergic asthma than among healthy controls (1.33±0.21 vs. 4.74±0.62, t=5.22, P < 0.05). Stimulation with dermatophagoides farinae extract (DFE) resulted in a reduction in miR-142-3p expression in BEAS-2B cells (0.82±0.25), while transfection with miR-142-3p mimics resulted in a rise in miR-142-3p expression in BEAS-2B cells (0.55±0.14)(t=3.31, 3.94, P < 0.05). Pre-treatment with miR-142-3p reduced the expression of IL-6(2.25±0.46)and TNF-α(6.58±1.95) (t=4.86, 3.38, P < 0.05) in BEAS-2B cells stimulated with DFE, and treatment with miR-142-3p mimics resulted in a reduction in TLR4 and NF-κB expression in BEAS-2B cells via negative regulation of the HMGB1 expression. In addition, treatment with miR-142-3p was found to alleviate inflammatory cell infiltration in lung tissues of house dust mite-sensitized mice, and results in a reduction in interleukin-4 (IL-4)[(107.60±10.43)pg/mL], interleukin-5 (IL-5)[(95.78±13.14)pg/mL] and HMGB1[(2.52±0.87)pg/mL] expression in BALF (t=10.32, 7.29, 2.90, P < 0.05). Conclusion miR-142-3p alleviates house dust mite-induced allergic airway inflammation among children via negative regulation of the HMGB1/TLR4/NF-κB pathway.
- Dermatophagoides farinae,
- MicroRNAs,
- High mobility group box 1 protein,
- Anaphylaxis,
- Respiratory tract diseases,
- Child

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References(27)

References

[1]	HOLGATE S T, WENZEL S, POSTMA D S, et al. Asthma[J]. Nat Rev Dis Primers, 2015, 1(1): 15025. doi: 10.1038/nrdp.2015.25
[2]	HUANG K, YANG T, XU J, et al. Prevalence, risk factors, and management of asthma in China: a national cross-sectional study[J]. Lancet, 2019, 394(10196): 407-418. doi: 10.1016/S0140-6736(19)31147-X
[3]	KANAGARATHAM C, RADZIOCH D. Allergic asthma: a summary from genetic basis, mouse studies, to diagnosis and treatment[J]. Curr Pharm Des, 2016, 22(41): 6261-6272. doi: 10.2174/1381612822666160829141708
[4]	THOMAS W R, HALES B J, SMITH W A. House dust mite allergens in asthma and allergy[J]. Trends Mol Med, 2010, 16(7): 321-328. doi: 10.1016/j.molmed.2010.04.008
[5]	SHIPP C L, GERGEN P J, GERN J E, et al. Asthma management in children[J]. J Allergy Clin Immunol Pract, 2023, 11(1): 9-18. doi: 10.1016/j.jaip.2022.10.031
[6]	GAN H, LUO W, HUANG Z, et al. House dust mite components sensitization profile in China, a multi-centre study[J]. Clin Exp Allergy, 2023, 53(2): 226-229. doi: 10.1111/cea.14255
[7]	SALIMINEJAD K, KHORRAM KHORSHID H R, SOLEYMANI FA-RD S, et al. An overview of microRNAs: biology, functions, therapeutics, and analysis methods[J]. J Cell Physiol, 2019, 234(5): 5451-5465. doi: 10.1002/jcp.27486
[8]	WANG X, GUO Y, WANG C, et al. microRNA-142-3p inhibits cho-ndrocyte apoptosis and inflammation in osteoarthritis by targeting HMGB1[J]. Inflammation, 2016, 39(5): 1718-1728. doi: 10.1007/s10753-016-0406-3
[9]	WANG Y, LIANG J, QIN H, et al. Elevated expression of miR-142-3p is related to the pro-inflammatory function of monocyte-derived dendritic cells in SLE[J]. Arthritis Res Ther, 2016, 18(1): 263. doi: 10.1186/s13075-016-1158-z
[10]	WU M, HUANG Z, HUANG W, et al. microRNA-124-3p attenuates myocardial injury in sepsis via modulating SP1/HDAC4/HIF-1α axis[J]. Cell Death Discov, 2022, 8(1): 40. doi: 10.1038/s41420-021-00763-y
[11]	GUIOT J, CAMBIER M, BOECKX A, et al. Macrophage-derived exosomes attenuate fibrosis in airway epithelial cells through delivery of antifibrotic miR-142-3p[J]. Thorax, 2020, 75(10): 870-881. doi: 10.1136/thoraxjnl-2019-214077
[12]	KLEINJAN A. Airway inflammation in asthma: key players beyond the Th2 pathway[J]. Curr Opin Pulm Med, 2016, 22(1): 46-52. doi: 10.1097/MCP.0000000000000224
[13]	DAVIS J D, WYPYCH T P. Cellular and functional heterogeneity of the airway epithelium[J]. Mucosal Immunol, 2021, 14(5): 978-990. doi: 10.1038/s41385-020-00370-7
[14]	LIVAK K J, SCHMITTGEN T D. Analysis of relative gene expression data using real-time quantitative PCR and the 2[-Delta Delta C(T)] Method[J]. Methods, 2001, 25(4): 402-408. doi: 10.1006/meth.2001.1262
[15]	BEREDA G. Bronchial asthma: etiology, pathophysiology, diagnosis and management[J]. Austin J Pulm Respir Med, 2022, 9(1): 1085.
[16]	LI X, SONG P, ZHU Y, et al. The disease burden of childhood asthma in China: a systematic review and Meta-analysis[J]. J Glob Health, 2020, 10(1): 010801. doi: 10.7189/jogh.10.010801
[17]	MAUER Y, TALIERCIO R M. Managing adult asthma: the 2019 GINA guidelines[J]. Cleve Clin J Med, 2020, 87(9): 569-575. doi: 10.3949/ccjm.87a.19136
[18]	SIMONEAU T, CLOUTIER M M. Controversies in pediatric asthma[J]. Pediatr Ann, 2019, 48(3): e128-e134.
[19]	WEIDNER J, BARTEL S, KILIÇ A, et al. Spotlight on microRNAs in allergy and asthma[J]. Allergy, 2021, 76(6): 1661-1678. doi: 10.1111/all.14646
[20]	QING X, ZHANG Y, PENG Y, et al. Mir-142-3p regulates inflammatory response by contributing to increased TNF-α in chronic rhinosinusitis with nasal polyposis[J]. Ear Nose Throat J, 2021, 100(1): NP50-NP56. doi: 10.1177/0145561319847972
[21]	BARTEL S, CARRARO G, ALESSANDRINI F, et al. miR-142-3p is associated with aberrant WNT signaling during airway remodeling in asthma[J]. Am J Physiol Lung Cell Mol Physiol, 2018, 315(2): L328-L333. doi: 10.1152/ajplung.00113.2018
[22]	WANG J Y, DONG X, YU Z, et al. Borneol inhibits CD4⁺ T cells proliferation by down-regulating miR-26a and miR-142-3p to attenuate asthma[J]. Int Immunopharmacol, 2021, 90: 107223. doi: 10.1016/j.intimp.2020.107223
[23]	DUMITRIU I E, BARUAH P, MANFREDI A A, et al. HMGB1: an immmune odyssey[J]. Discov Med, 2005, 5(28): 388-392.
[24]	ZHAO Y, LI R. HMGB1 is a promising therapeutic target for asthma[J]. Cytokine, 2023, 165: 156171. doi: 10.1016/j.cyto.2023.156171
[25]	KO H K, HSU W H, HSIEH C C, et al. High expression of high-mobility group box 1 in the blood and lungs is associated with the development of chronic obstructive pulmonary disease in smokers[J]. Respirology, 2014, 19(2): 253-261. doi: 10.1111/resp.12209
[26]	CHENG Y, WANG D, WANG B, et al. HMGB1 translocation and release mediate cigarette smoke-induced pulmonary inflammation in mice through a TLR4/MyD88-dependent signaling pathway[J]. Mol Biol Cell, 2017, 28(1): 201-209. doi: 10.1091/mbc.e16-02-0126
[27]	HUANG W F, ZHAO H J, DONG H M, et al. High-mobility group box 1 impairs airway epithelial barrier function through the activation of the RAGE/ERK pathway[J]. Int J Mol Med, 2016, 37(5): 1189-1198. doi: 10.3892/ijmm.2016.2537