Antagonistic effect of vitamin E on nAl2O3-induced exacerbation of Th2 and Th17-mediated allergic asthma via oxidative stress

Cui, Haiyan; Huang, Jiawei; Lu, Manman; Zhang, Qian; Qin, Wei; Zhao, Yun; Lu, Xianxian; Zhang, Jiting; Xi, Zhuge; Li, Rui

doi:10.1016/j.envpol.2019.06.092

Cited by 19 publications

(14 citation statements)

References 49 publications

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“…The imbalance of Th17 and Treg is implicated in many allergic diseases in respiratory system [52,53]. Especially, Th17 mediated inflammatory responses are crucial for the onset, exacerbation and control of Asthma and Chronic Obstructive Pulmonary Disease [54][55][56][57][58][59]. The role of STAT3 in Treg/Th17 imbalance in widely reported for allergic diseases.…”

Section: Discussionmentioning

confidence: 99%

IRF4 and STAT3 activities are associated with the imbalanced differentiation of T-cells in responses to inhalable particulate matters

Zhong

et al. 2020

Respir Res

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Background: Particulate Matter (PM) is known to cause inflammatory responses in human. Although prior studies verified the immunogenicity of PM in cell lines and animal models, the effectors of PM exposure in the respiratory system and the regulators of the immunogenicity of PM is not fully elucidated. Methods: To identify the potential effector of PM exposure in human respiratory system and to better understand the biology of the immunogenicity of PM, We performed gene-expression profiling of peripheral blood mononuclear cells from 171 heathy subjects in northern China to identify co-expressed gene modules associated with PM exposure. We inferred transcription factors regulating the co-expression and validated the association to Tcell differentiation in both primary T-cells and mice treated with PM. Results: We report two transcription factors, IRF4 and STAT3, as regulators of the gene expression in response to PM exposure in human. We confirmed that the activation of IRF4 and STAT3 by PM is strongly associated with imbalanced differentiation of T-cells in the respiratory tracts in a time-sensitive manner in mouse. We also verified the consequential inflammatory responses of the PM exposure. Moreover, we show that the protein levels of phosphorylated IRF4 and STAT3 increase with PM exposure. Conclusions: Our study suggests the regulatory activities of IRF4 and STAT3 are associated with the Th17-mediated inflammatory responses to PM exposure in the respiratory tracts, which informs the biological background of the immunogenicity of particulate matters.

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Section: Discussionmentioning

confidence: 99%

IRF4 and STAT3 activities are associated with the imbalanced differentiation of T-cells in responses to inhalable particulate matters

Zhong

et al. 2020

Respir Res

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“…Similarly, anti-IL-23 monoclonal therapy may be effective in eliminating the 17 cell-eosinophil axis [51]. A simpler treatment may be used to inhibit eosinophil peroxidase with antioxidants such as vitamin E, limiting the main factors that cause the damage observed in these studies [51,117]. Gallic acid treatment downregulated the expression of RORct and IL-17 [71].…”

Section: Future Diagnosis and Treatment Optionsmentioning

confidence: 99%

The Role of Th17 Cells and IL-17 in Th2 Immune Responses of Allergic Conjunctivitis

Meng

Shi

Zhang

et al. 2020

Journal of Ophthalmology

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Allergic conjunctivitis (AC) is a common allergic disease that is often associated with the onset of rhinitis or asthma. The incidence of AC has increased significantly in recent years possibly due to air pollution and climate warming. AC seriously affects patients’ quality of life and work efficiency. Th (T-helper) 2 immune responses and type I hypersensitivity reactions are generally considered the basis of occurrence of AC. It has been found that new subpopulations of T-helper cells, Th17 cells that produce interleukin-17 (IL-17), play an important role in the Th2-mediated pathogenesis of conjunctivitis. Studies have shown that Th17 cells are involved in a variety of immune inflammation, including psoriasis, rheumatoid arthritis, inflammatory bowel disease, systemic lupus erythematosus, and asthma. However, the role of Th17 and IL-17 in AC is unclear. This paper will focus on how T-helper 17 cells and interleukin-17 are activated in the Th2 immune response of allergic conjunctivitis and how they promote the Th2 immune response of AC.

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“…Previous studies have shown that VitD, VitE, folic acid and other vitamins can regulate allergic airway inflammation during the pathogenic process of allergic asthma [12][13][14], but the precise role of maternal VitD deficiency in offspring has not been clarified. Our data highlighted that maternal female mice with long-term lower VitD diet not only caused VitD deficiency in the recipients, but also induced VitD deficiency in their offspring even after fed with normal chow for couple weeks.…”

Section: Discussionmentioning

confidence: 99%

Maternal vitamin D deficiency impairs Treg and Breg responses in offspring mice and deteriorates allergic airway inflammation

Huang

Wang

et al. 2020

Allergy Asthma Clin Immunol

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Background Vitamin D (VitD) can regulate immune responses and maternal VitD-deficiency can affect immune responses in the offspring. This study aimed at investigating the effects of maternal VitD-deficiency during pregnancy on Treg and Breg responses in offspring mice with house dust mite (HDM)-induced allergic airway inflammation. Methods Female BALB/c mice were randomized and fed with normal chow or VitD-deficient diet until their offspring weaned. The offspring mice were fed with normal chow and injected with vehicle or HDM to induce allergic airway inflammation. The levels of serum 25(OH)D, cytokines and infiltrate numbers as well as percentages of Tregs and Bregs in the bronchoalveolar lavage fluid (BALF) were analyzed. The relative levels of VitD receptor (VDR), VitD-binding protein (VDBP), Cytochromes P450 (CYP) 27b1, and CYP24A1 mRNA transcripts in the lungs of different groups of mice were measured. Results Maternal VitD-deficiency significantly reduced serum 25(OH)D levels in offspring mice. VitD-deficiency significantly increased the relative levels of VDR, VDBP and CYP27B1 mRNA transcripts, but decreased CYP24A1 expression in the lungs of mice. In comparison with the control mice, significantly elevated levels of pro-inflammatory cytokines, increased numbers of lymphocytes and eosinophils, but decreased levels of anti-inflammatory cytokines were detected in the BALF of VitD-deficient mice. VitD-deficiency significantly increased the frequency of Th1, Th2, Th9, Th17 cells, but decreased regulatory T (Tregs) and B cells (Bregs) in the BALF of mice with allergic airway inflammation. Conclusion Maternal VitD-deficiency lowed serum 25(OH)D levels and enhanced HDM-induced allergic airway inflammation in the offspring by impairing Breg and Treg responses.

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Antagonistic effect of vitamin E on nAl2O3-induced exacerbation of Th2 and Th17-mediated allergic asthma via oxidative stress

Cited by 19 publications

References 49 publications

IRF4 and STAT3 activities are associated with the imbalanced differentiation of T-cells in responses to inhalable particulate matters

IRF4 and STAT3 activities are associated with the imbalanced differentiation of T-cells in responses to inhalable particulate matters

The Role of Th17 Cells and IL-17 in Th2 Immune Responses of Allergic Conjunctivitis

Maternal vitamin D deficiency impairs Treg and Breg responses in offspring mice and deteriorates allergic airway inflammation

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