Regulatory effect of glutathione on treg/Th17 cell balance in allergic rhinitis patients through inhibiting intracellular autophagy

Fan, Yuqin; Yang, Chenchen; Zhou, Jieyu; Cheng, Xuefeng; Dong, Yu; Wang, Qin; Wang, Zhentao

doi:10.1080/08923973.2020.1850762

Cited by 16 publications

(15 citation statements)

References 32 publications

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“…Preceding studies proposed that AR induced Treg/Th17 imbalance. 6,24 As a result, levels of the Treg cell cytokines IL-10 and Foxp3 as well as the Th17 cell cytokines IL-17 and TGF-β in guinea pig tissues or serum were examined. The testing results revealed that IL-10 and Foxp3 levels were declined whereas IL-17 and TGF-β levels were increased ( p < 0.05, Figure 1(G) to (N)).…”

Section: Resultsmentioning

confidence: 99%

“…30 Of note, Treg cell reduction and Th17 cell amplification exist in AR patients and this imbalance is correlated with AR progression. 6 On a separate note, a former review by Rahim et al highlighted that extracts derived from certain medicinal plants possess an anti-AR effect. 31 APS derived from Astragalus membranaceus has various pharmacological properties and is regarded as a plant component with promising potential to improve or treat multiple diseases.…”

Section: Discussionmentioning

confidence: 99%

“…4,5 Moreover, Treg/Th17 imbalance is proposed as a one pathogenesis of AR and is closely implicated in AR progression. 6 Hence, it is prudent and imperative to conduct an in-depth investigation on inflammatory responses and Treg/Th17 imbalance in AR.…”

Section: Introductionmentioning

confidence: 99%

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Astragalus Polysaccharide Relieves Inflammatory Responses in Guinea Pigs with Allergic Rhinitis via Ameliorating NF-kB-Mediated Treg/Th17 Imbalance

Liu

Luo

et al. 2022

Am J Rhinol�Allergy

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Background Allergic rhinitis (AR) is regarded as a prevalent and non-infectious inflammation in nasal mucosa, and astragalus polysaccharide (APS) could mitigate inflammation. Objectives Herein, this study probed the specific mechanism of APS in inflammatory responses in AR. Methods Firstly, AR guinea pig models were established through the stimulation and sensitization of ovalbumin (OVA) and received APS treatment. Changes in nasal symptoms were assessed through counting the sneezing and rubbing times of guinea pigs. The change patterns of OVA-specific immunoglobulin-E (OVA-sIgE), OVA-specific immunoglobulin-G1 (OVA-sIgG1), tumor necrosis factor (TNF)-α, and interleukin (IL)-6 in guinea pig serum were identified. Meanwhile, the levels of IL-17, transforming growth factor (TGF)-β, IL-10, and forkhead box protein P3 (Foxp3) in the guinea pig tissues or serum were examined, and CD25+Foxp3+Treg or CD4+IL17+Th17 cell proportion was detected. Afterwards, nuclear factor-kappa B (NF-kB) expression in guinea pig nasal mucosa tissues were examined. Rescue experiments were designed to probe the role of NF-kB overexpression in inflammatory responses and Treg/Th17 imbalance in AR guinea pigs. Results APS treatment reduced sneezing and rubbing times of AR guinea pigs and suppressed OVA-sIgE, OVA-sIgG1, TNF-α, and IL-6 levels in guinea pig serum, and meanwhile, increased CD25+Foxp3+Treg cell proportion while reduced CD4+IL17+Th17 cell proportion in AR guinea pig serum or tissues, in a dose-dependent manner. NF-kB was highly-expressed in AR guinea pigs and down-regulated after APS treatment. NF-kB overexpression facilitated inflammatory responses and Treg/Th17 imbalance in AR. Conclusion APS reduced Treg/Th17 imbalance via suppressing NF-kB expression, thereby ameliorating inflammatory responses in AR.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Astragalus Polysaccharide Relieves Inflammatory Responses in Guinea Pigs with Allergic Rhinitis via Ameliorating NF-kB-Mediated Treg/Th17 Imbalance

Liu

Luo

et al. 2022

Am J Rhinol�Allergy

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“…8 Antisense non-coding RNA in the INK4 locus (ANRIL), also known as CDKN2B-AS1, is a lncRNA encoded in the chromosome 9p21 region, which is related with risk increase, severity and inflammatory status of AR. 9 Previous preliminary studies have found that AR progression was closely related with the cell autophagy, 10,11 and ANRIL was reported to be related with cell autophagy. 12,13 For instance, lncRNA ANRIL could aggravate the chemoresistance of pancreatic cancer cells to gemcitabine by targeting HMGB1-induced autophagy 14 ; ANRIL could mitigate neonatal hypoxic-ischemic brain damage via promoting the autophagy.…”

Section: Introductionmentioning

confidence: 97%

LncRNA ANRIL Promotes Autophagy Activation Through miR-16-5p/TLR4 Axis in Allergic Rhinitis

Wang

Zhu

Liu

et al. 2022

Am J Rhinol�Allergy

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Background Allergic rhinitis (AR) is an allergic disease of nasal mucosa. LncRNAs are key modulators affecting AR development. Neverthelss, the impact of lncRNA ANRIL in AR is not clear. Objective This work decided to study the mechanism underlying the impact of ANRIL on TLR4 expression through targeting miR-16-5p during autophagy and epithelial barrier dysfunction in the progression of AR. Methods Human nasal epithelial cells were exposed to TNF-α to establish AR cell model, AR mice model was constructed by ovalbumin (OVA) treatment. QRT-PCR or western blot assays were applied to measure the levels of mRNA and proteins. Dual-luciferase reporter gene detection and RIP assay were conducted to verify the association between ANRIL and miR-16-5p. Autophagy flux assessment by mRFP-GFP-LC3 method was performed to detect autophagy level. Results AR progression could induce the autophagy, and the expressions of tight junction proteins were downregulated in AR cell model. Moreover, knockdown of ANRIL reversed the effect of AR on autophagy-related protein and tight junction proteins MiR-16-5p was found to be bound with ANRIL and miR-16-5p inhibitor could reverse ANRIL knockdown-induced downregulation of autophagy-related proteins and epithelial barrier dysfunction. In addition, miR-16-5p directly targeted TLR4. Furthermore, knockdown of ANRIL reversed miR-16-5p and TLR4 expression, autophagy level, and tight junction protein levels in nasal mucosa of AR mice. Conclusion This study illustrated that ANRIL acted as a promotion factor in AR induced autophagy and epithelial barrier dysfunction by enhancing the expression of TLR4 via interacting with miR-16-5p.

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“…It is well established that T-helper (Th)1/Th2 imbalance has a critical role in the pathogenesis of AR, characterized by Th2 cell-mediated inflammatory response [6]. Recently, the critical role of regulatory T (Treg)/Th17 cell-mediated immunity imbalance has also been identified in AR patients [7][8][9]. Treg cell is a subset of T lymphocytes implicated in allergic conditions, which can modulate the pathophysiological immune response, promote autoimmune tolerance, and maintain immune balance [10].…”

Section: Introductionmentioning

confidence: 99%

Mechanism of miR-181a-5p in Regulatory T/T-Helper 17 Immune Imbalance and Asthma Development in Mice with Allergic Rhinitis

Chen

et al. 2021

Int Arch Allergy Immunol

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Introduction: Allergic rhinitis (AR) is an immune disorder and also a risk factor of asthma. microRNAs (miRNAs) are implicated in autoimmune diseases, including RA. This study investigated effect of miR-181a-5p on regulatory T (Treg)/ T-helper (Th) 17 immune imbalance in AR. Methods: A murine model of AR was established and treated with lentivirus modified miR-181a-5p. The allergic symptoms of mice were examined. The contents of Th17-related cytokines (interferon [IFN]-γ and interleukin [IL]-6), Treg-related cytokine (IL-10), and Treg-specific nuclear transcription factor (Foxp3) in nasal mucosa and lung tissues were determined. The proportion of Treg and Th17 cells was analyzed by flow cytometry. The level of ovalbumin-specific immunoglobulin E in the serum, and the contents of IL-4, IL-5, and IL-13 in bronchoalveolar lavage fluid and IFN-γ, IL-6, and IL-10 in nasal lavage fluid were measured. The targeting relationship between miR-181a-5p and high mobility group box chromosomal protein 1 (HMGB1) was verified. HMGB1 and receptor for advanced glycation end products (RAGE) expression in RA were determined, and the interaction between HMGB1 and RAGE was detected. Results: miR-181a-5p expression was reduced in AR mice. miR-181a-5p overexpression attenuated allergic behaviors, alleviated Treg/Th17 imbalance, and delayed asthma development. HMGB1 and RAGE were elevated in AR mice. miR-181a-5p targeted HMGB1, and HMGB1 bound to RAGE, while miR-181a-5p overexpression reduced the binding between them. Activating HMGB1/RAGE reversed the protective effect of miR-181a-5p overexpression on AR and induced the development of asthma. Conclusion: miR-181a-5p overexpression reduced the binding of HMGB1 and RAGE by inhibiting HMGB1, thus alleviating Treg/Th17 immune imbalance and blocking AR from developing into asthma.

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Regulatory effect of glutathione on treg/Th17 cell balance in allergic rhinitis patients through inhibiting intracellular autophagy

Cited by 16 publications

References 32 publications

Astragalus Polysaccharide Relieves Inflammatory Responses in Guinea Pigs with Allergic Rhinitis via Ameliorating NF-kB-Mediated Treg/Th17 Imbalance

Astragalus Polysaccharide Relieves Inflammatory Responses in Guinea Pigs with Allergic Rhinitis via Ameliorating NF-kB-Mediated Treg/Th17 Imbalance

LncRNA ANRIL Promotes Autophagy Activation Through miR-16-5p/TLR4 Axis in Allergic Rhinitis

Mechanism of miR-181a-5p in Regulatory T/T-Helper 17 Immune Imbalance and Asthma Development in Mice with Allergic Rhinitis

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