scholarly journals Illicium verum Extract and Trans-Anethole Attenuate Ovalbumin-Induced Airway Inflammation via Enhancement of Foxp3+ Regulatory T Cells and Inhibition of Th2 Cytokines in Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Yoon-Young Sung ◽  
Seung-Hyung Kim ◽  
Dong-Seon Kim ◽  
Ji-eun Lee ◽  
Ho Kyoung Kim
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Airway Inflammation ◽  
Airway Hyperresponsiveness ◽  
Cytokine Production ◽  
Foxp3 Expression ◽  
Eosinophilic Infiltration ◽  
Th2 Cytokines ◽  
Th2 Cytokine ◽  
Illicium Verum

Illicium verum is used in traditional medicine to treat inflammation. The study investigates the effects of IVE and its component, trans-anethole (AET), on airway inflammation in ovalbumin- (OVA-) induced asthmatic mice. Asthma was induced in BALB/c mice by systemic sensitization to OVA, followed by intratracheal, intraperitoneal, and aerosol allergen challenges. IVE and AET were orally administered for four weeks. We investigated the effects of treatment on airway hyperresponsiveness, IgE production, pulmonary eosinophilic infiltration, immune cell phenotypes, Th2 cytokine production in bronchoalveolar lavage, Th1/Th2 cytokine production in splenocytes, forkhead box protein 3 (Foxp3) expression, and lung histology. IVE and AET ameliorated OVA-driven airway hyperresponsiveness (p<0.01), pulmonary eosinophilic infiltration (p<0.05), mucus hypersecretion (p<0.01), and IL-4, IL-5, IL-13, and CCR3 production (p<0.05), as well as IgE levels (p<0.01). IVE and AET increased Foxp3 expression in lungs (p<0.05). IVE and AET reduced IL-4 and increased IFN-γ production in the supernatant of splenocyte cultures (p<0.05). Histological studies showed that IVE and AET inhibited eosinophilia and lymphocyte infiltration in lungs (p<0.01). These results indicate that IVE and AET exert antiasthmatic effects through upregulation of Foxp3+ regulatory T cells and inhibition of Th2 cytokines, suggesting that IVE may be a potential therapeutic agent for allergic lung inflammation.

scholarly journals Glucocorticoid hormone treatment enhances the cytokine production of regulatory T cells by upregulation of Foxp3 expression

Immunobiology ◽  
2018 ◽  
Vol 223 (4-5) ◽  
pp. 422-431 ◽  
Author(s):  
Emese Ugor ◽  
Lilla Prenek ◽  
Ramóna Pap ◽  
Gergely Berta ◽  
Dávid Ernszt ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Cytokine Production ◽  
Foxp3 Expression ◽  
Hormone Treatment ◽  
Glucocorticoid Hormone

scholarly journals Nonfunctional Regulatory T Cells and Defective Control of Th2 Cytokine Production in Natural Scurfy Mutant Mice

2009 ◽  
Vol 183 (9) ◽  
pp. 5662-5672 ◽  
Author(s):  
Katharina Lahl ◽  
Christian T. Mayer ◽  
Tobias Bopp ◽  
Jochen Huehn ◽  
Christoph Loddenkemper ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Cytokine Production ◽  
Mutant Mice ◽  
Th2 Cytokine

scholarly journals Critical role of CD28/B7 costimulation in the development of human Th2 cytokine-producing cells

Blood ◽  
1995 ◽  
Vol 86 (9) ◽  
pp. 3479-3486 ◽  
Author(s):  
LM Webb ◽  
M Feldmann
Keyword(s):  
T Cells ◽  
Cytokine Production ◽  
Critical Role ◽  
Th2 Cytokines ◽  
T Helper ◽  
Cd4 Cells ◽  
Th2 Cytokine ◽  
Cd28 Costimulation ◽  
Costimulatory Pathway

CD28 is a major costimulatory signal receptor for T cells. We have used human naive CD4+ cells from cord blood to analyze the effect of the CD28/B7 costimulatory pathway on development of T helper (Th) subsets. We show that CD28 costimulation is critical for development of the Th2 cytokine-producing cells and that in the absence of CD28 costimulation, cells are not primed to produce Th2 cytokines and consequently “default” to the Th1 subset, independent of the presence of exogenous cytokines. After CD28 costimulation, cells differentiate into a subset that produces Th2 cytokines. However, further CD28 costimulation is not required to maintain Th2 cytokine production. We conclude that D28 costimulation is critical for the development of Th0 and Th2 subsets, but not for the maintenance of cytokine production.

scholarly journals High Th2 cytokine levels and upper airway inflammation in human inherited T-bet deficiency

2021 ◽  
Vol 218 (8) ◽  
Author(s):  
Rui Yang ◽  
Marc Weisshaar ◽  
Federico Mele ◽  
Ibtihal Benhsaien ◽  
Karim Dorgham ◽  
...  
Keyword(s):  
T Cells ◽  
Airway Inflammation ◽  
Upper Airway ◽  
Th2 Cells ◽  
Mutant Form ◽  
Th2 Cytokines ◽  
Blood Eosinophilia ◽  
Th2 Cytokine ◽  
Ifn Γ ◽  
Αβ T Cells

We have described a child suffering from Mendelian susceptibility to mycobacterial disease (MSMD) due to autosomal recessive, complete T-bet deficiency, which impairs IFN-γ production by innate and innate-like adaptive, but not mycobacterial-reactive purely adaptive, lymphocytes. Here, we explore the persistent upper airway inflammation (UAI) and blood eosinophilia of this patient. Unlike wild-type (WT) T-bet, the mutant form of T-bet from this patient did not inhibit the production of Th2 cytokines, including IL-4, IL-5, IL-9, and IL-13, when overexpressed in T helper 2 (Th2) cells. Moreover, Herpesvirus saimiri–immortalized T cells from the patient produced abnormally large amounts of Th2 cytokines, and the patient had markedly high plasma IL-5 and IL-13 concentrations. Finally, the patient’s CD4+ αβ T cells produced most of the Th2 cytokines in response to chronic stimulation, regardless of their antigen specificities, a phenotype reversed by the expression of WT T-bet. T-bet deficiency thus underlies the excessive production of Th2 cytokines, particularly IL-5 and IL-13, by CD4+ αβ T cells, causing blood eosinophilia and UAI. The MSMD of this patient results from defective IFN-γ production by innate and innate-like adaptive lymphocytes, whereas the UAI and eosinophilia result from excessive Th2 cytokine production by adaptive CD4+ αβ T lymphocytes.

scholarly journals Resolution of airway inflammation and hyperreactivity after in vivo transfer of CD4+CD25+ regulatory T cells is interleukin 10 dependent

2005 ◽  
Vol 202 (11) ◽  
pp. 1539-1547 ◽  
Author(s):  
Jennifer Kearley ◽  
Jane E. Barker ◽  
Douglas S. Robinson ◽  
Clare M. Lloyd
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Airway Inflammation ◽  
Intracellular Cytokine Staining ◽  
Allergen Challenge ◽  
Interleukin 10 ◽  
Airway Hyperreactivity ◽  
Th2 Cytokine ◽  
Th2 Cell

Deficient suppression of T cell responses to allergen by CD4+CD25+ regulatory T cells has been observed in patients with allergic disease. Our current experiments used a mouse model of airway inflammation to examine the suppressive activity of allergen-specific CD4+CD25+ T cells in vivo. Transfer of ovalbumin (OVA) peptide–specific CD4+CD25+ T cells to OVA-sensitized mice reduced airway hyperreactivity (AHR), recruitment of eosinophils, and T helper type 2 (Th2) cytokine expression in the lung after allergen challenge. This suppression was dependent on interleukin (IL) 10 because increased lung expression of IL-10 was detected after transfer of CD4+CD25+ T cells, and regulation was reversed by anti–IL-10R antibody. However, suppression of AHR, airway inflammation, and increased expression of IL-10 were still observed when CD4+CD25+ T cells from IL-10 gene–deficient mice were transferred. Intracellular cytokine staining confirmed that transfer of CD4+CD25+ T cells induced IL-10 expression in recipient CD4+ T cells, but no increase in IL-10 expression was detected in airway macrophages, dendritic cells, or B cells. These data suggest that CD4+CD25+ T cells can suppress the Th2 cell–driven response to allergen in vivo by an IL-10–dependent mechanism but that IL-10 production by the regulatory T cells themselves is not required for such suppression.

scholarly journals Regulatory T Cells Accumulate in the Lung Allergic Inflammation and Efficiently Suppress T-Cell Proliferation but Not Th2 Cytokine Production

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Lucas Faustino ◽  
Daniel Mucida ◽  
Alexandre Castro Keller ◽  
Jocelyne Demengeot ◽  
Karina Bortoluci ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cells ◽  
T Cell ◽  
Regulatory T Cells ◽  
Cytokine Production ◽  
Allergic Inflammation ◽  
Peripheral Tolerance ◽  
Effector Memory ◽  
T Cell Proliferation ◽  
Th2 Cytokine

Foxp3+CD25+CD4+regulatory T cells are vital for peripheral tolerance and control of tissue inflammation. In this study, we characterized the phenotype and monitored the migration and activity of regulatory T cells present in the airways of allergic or tolerant mice after allergen challenge. To induce lung allergic inflammation, mice were sensitized twice with ovalbumin/aluminum hydroxide gel and challenged twice with intranasal ovalbumin. Tolerance was induced by oral administration of ovalbumin for 5 consecutive days prior to OVA sensitization and challenge. We detected regulatory T cells (Foxp3+CD25+CD4+T cells) in the airways of allergic and tolerant mice; however, the number of regulatory T cells was more than 40-fold higher in allergic mice than in tolerant mice. Lung regulatory T cells expressed an effector/memory phenotype (CCR4highCD62LlowCD44highCD54highCD69+) that distinguished them from naive regulatory T cells (CCR4intCD62LhighCD44intCD54intCD69−). These regulatory T cells efficiently suppressed pulmonary T-cell proliferation but not Th2 cytokine production.

scholarly journals Adipose-Derived Stem Cells Ameliorate Allergic Airway Inflammation by Inducing Regulatory T Cells in a Mouse Model of Asthma

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Kyu-Sup Cho ◽  
Mi-Kyung Park ◽  
Shin-Ae Kang ◽  
Hee-Young Park ◽  
Sung-Lyong Hong ◽  
...  
Keyword(s):  
Stem Cells ◽  
T Cells ◽  
Regulatory T Cells ◽  
Bronchoalveolar Lavage ◽  
Airway Inflammation ◽  
Bronchoalveolar Lavage Fluid ◽  
Immune Cell ◽  
Allergic Airway Inflammation ◽  
Lavage Fluid ◽  
Th2 Cytokines

Although several studies have demonstrated that mesenchymal stem cells derived from adipose tissue (ASCs) can ameliorate allergic airway inflammation, the immunomodulatory mechanism of ASCs remains unclear. In this study, we investigated whether regulatory T cells (Tregs) induction is a potential mechanism in immunomodulatory effects of ASCs on allergic airway disease and how these induced Tregs orchestrate allergic inflammation. Intravenous administration of ASCs significantly reduced allergic symptoms and inhibited eosinophilic inflammation. Airway hyperresponsiveness, total immune cell and eosinophils in the bronchoalveolar lavage fluid, mucus production, and serum allergen-specific IgE and IgG1 were significantly reduced after ASCs administration. ASCs significantly inhibited Th2 cytokines (IL-4, IL-5, and IL-13) and enhanced Th1 cytokine (IFN-γ) and regulatory cytokines (IL-10 and TGF-β) in the bronchoalveolar lavage fluid and lung draining lymph nodes. Furthermore, levels of IDO, TGF-β, and PGE2were significantly increased after ASCs administration. Interestingly, this upregulation was accompanied by increased Treg populations. In conclusion, ASCs ameliorated allergic airway inflammation and improved lung function through the induction of Treg expansion. The induction of Treg by ASCs involves the secretion of soluble factors such as IDO, TGF-β, and PGE2and Treg might be involved in the downregulation of Th2 cytokines and upregulation of Th1 cytokines production.

scholarly journals Antiasthmatic Effects of Hesperidin, a Potential Th2 Cytokine Antagonist, in a Mouse Model of Allergic Asthma

2011 ◽  
Vol 2011 ◽  
pp. 1-12 ◽  
Author(s):  
Seung-Hyung Kim ◽  
Bok-Kyu Kim ◽  
Young-Cheol Lee
Keyword(s):  
Mouse Model ◽  
Airway Inflammation ◽  
Airway Hyperresponsiveness ◽  
Immune Cell ◽  
Airflow Obstruction ◽  
Specific Ige ◽  
Eosinophil Infiltration ◽  
Th2 Cytokines ◽  
Th2 Cytokine

Background and Objective. The features of asthma are airway inflammation, reversible airflow obstruction, and an increased sensitivity to bronchoconstricting agents, termed airway hyperresponsiveness (AHR), excess production of Th2 cytokines, and eosinophil accumulation in the lungs. To investigate the antiasthmatic potential of hesperidin as well as the underlying mechanism involved, we studied the inhibitory effect and anti-inflammatory effect of hesperidin (HPN) on the production of Th2 cytokines, eotaxin, IL-17, -OVA-specific IgEin vivoasthma model mice.Methods. In this paper, BALB/c mice were systemically sensitized to ovalbumin (OVA) followed intratracheally, intraperitoneally, and by aerosol allergen challenges. We investigated the effect of HPN on airway hyperresponsiveness, pulmonary eosinophilic infiltration, various immune cell phenotypes, Th2 cytokine production and OVA-specific IgE production in a mouse model of asthma.Results. In BALB/c mice, we found that HPN-treated groups had suppressed eosinophil infiltration, allergic airway inflammation, and AHR, and these occurred by suppressing the production of IL-5, IL-17, and OVA-specific IgE.Conclusions. Our data suggest that the therapeutic mechanism by which HPN effectively treats asthma is based on reductions of Th2 cytokines (IL-5), eotaxin, OVA-specific IgE production, and eosinophil infiltration via inhibition of GATA-3 transcription factor.

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