Effect of inhaled and systemic glucocorticoid treatment on CD4 + regulatory and effector T cells in a mouse model of allergic asthma

Zuśka-Prot, Monika; Maślanka, Tomasz

doi:10.1016/j.intimp.2017.02.005

Cited by 14 publications

(13 citation statements)

References 19 publications

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“…Hence, our findings may provide new insights into the pathogenesis of VitD deficiency-related allergic airway inflammation and theoretically, correction of VitD deficiency may be valuable in inhibiting the pathogenic process of allergic airway inflammation. It is well known that activated CD4 + T cells can differentiate into IFNγ-secreting Th1, IL-4/IL-5/IL-13secreting Th2, IL-17A-secreting Th17, IL-9-secreting Th9 and IL-10/TGFβ1-secreting Tregs, dependent on cytokines in the environment [2,25]. In addition, CD4 + FoxP3 + nature Tregs exist in the body.…”

Section: Discussionmentioning

confidence: 99%

“…These inflammatory cells and their cytokines work together to eventually induce and exacerbate the HDM-induced allergic airway inflammatory [2]. In contrast, Tregs can effectively inhibit the pathogenic process of HDM-induced allergic airway inflammation by secreting inhibitory IL-10 and TGFβ1 [3,25,31]. Actually, our previous studies and those of others have shown that Tregs can inhibit the activation of effector T cells and their cytokine secretion, and reduce mast cell, eosinophil, basophil and neutrophil infiltration in the lung [25,32].…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, Tregs can effectively inhibit the pathogenic process of HDM-induced allergic airway inflammation by secreting inhibitory IL-10 and TGFβ1 [3,25,31]. Actually, our previous studies and those of others have shown that Tregs can inhibit the activation of effector T cells and their cytokine secretion, and reduce mast cell, eosinophil, basophil and neutrophil infiltration in the lung [25,32]. Therefore, the imbalance of inflammatory cells and Tregs caused by VitD deficiency may be crucial for the development and progression of HDM-induced allergic airway inflammation.…”

Section: Discussionmentioning

confidence: 99%

“…It is well known that activated CD4 + T cells can differentiate into IFNγ-secreting Th1, IL-4/IL-5/IL-13-secreting Th2, IL-17A-secreting Th17, IL-9-secreting Th9 and IL-10/TGFβ1-secreting Tregs, dependent on cytokines in the environment [ 2 , 25 ]. In addition, CD4 + FoxP3 + nature Tregs exist in the body.…”

Section: Discussionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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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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“…However, both the incidence and prevalence of asthma remain high (Gershon et al, 2010). Studies suggest that inhaled GCs, similarly to those administered systemically, can lower the immune response toward various pathogens, both within and outside of the respiratory system (Zuska-Prot and Maslanka, 2017). Therefore, it is imperative that the mechanisms underlying this disease are further identified, and new therapies developed.…”

Section: Introductionmentioning

confidence: 99%

Modified Si–Jun–Zi–Tang Attenuates Airway Inflammation in a Murine Model of Chronic Asthma by Inhibiting Teff Cells via the mTORC1 Pathway

Jin

Cai

et al. 2019

Front. Pharmacol.

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Background: Modified Si–Jun–Zi–Tang (MSJZT), a multi-herb formulation, is frequently used in traditional Chinese medicine for patients during the remission stage of asthma. However, the pharmacological basis underlying the effects of MSJZT on asthma has yet to be elucidated. This study aims at evaluating the anti-asthmatic effects of MSJZT and investigating its possible mechanism. Methods: A chronic murine model of asthma was established by sensitization and repeated challenge with ovalbumin (OVA) in female BALB/c mice, followed with oral administration of MSJZT during remission, and then mouse were re-challenged by OVA. The chemical profile of MSJZT was analyzed by high-performance liquid chromatography. The characteristic features of allergic asthma, including airway hyperreactivity, histopathology, cytokine levels (IL-4, -5, -13, -17, and INF-γ), T regulatory (Treg) lymphocytes (Foxp3+CD4+CD25+), and T effector (Teff) lymphocytes (Foxp3-CD25+CD4+) in bronchoalveolar lavage fluid (BALF), and downstream proteins of mTORC1/2 signaling pathway were examined. Results: MSJZT markedly suppressed airway hyper-responsiveness to aerosolized methacholine, and reduced levels of IL-4, IL-5, and IL-13 in the BALF. Histological studies showed that MSJZT significantly reduced inflammatory infiltration in lung tissues. The percentage and absolute number of Teff cells were suppressed to a remarkable level by MSJZT without affecting Treg cells. Furthermore, MSJZT effectively inhibited the mTORC1 activity, but exerted limited effects on mTORC2, as assessed by the phosphorylation of the mTORC1 and mTORC2 substrates, S6 ribosomal protein, p70 S6 kinase, mTOR S2481, and Akt, respectively. Conclusion: MSJZT attenuated chronic airway inflammation in a mouse model of asthma by inhibiting Teff cells, which occurred, at least in part, via modulation of the mTORC1 signaling pathway.

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Schisandrin B promotes Foxp3+ regulatory T cell expansion by activating heme oxygenase-1 in dendritic cells and exhibits immunomodulatory effects in Th2-mediated allergic asthma

Chiang

Chang

Chuang

et al. 2022

European Journal of Pharmacology

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Effect of inhaled and systemic glucocorticoid treatment on CD4 + regulatory and effector T cells in a mouse model of allergic asthma

Cited by 14 publications

References 19 publications

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

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

Modified Si–Jun–Zi–Tang Attenuates Airway Inflammation in a Murine Model of Chronic Asthma by Inhibiting Teff Cells via the mTORC1 Pathway

Schisandrin B promotes Foxp3+ regulatory T cell expansion by activating heme oxygenase-1 in dendritic cells and exhibits immunomodulatory effects in Th2-mediated allergic asthma

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