Identification of atopic dermatitis phenotypes with good responses to probiotics (Lactobacillus plantarum CJLP133) in children

2017 ◽  
Vol 8 (5) ◽  
pp. 755-761 ◽  
Author(s):  
J. Kim ◽  
B.S. Lee ◽  
B. Kim ◽  
I. Na ◽  
J. Lee ◽  
...  

The therapeutic effect of probiotics in atopic dermatitis (AD) remains controversial and varies according to the individual patient. We aimed to identify a population of AD patients with a good clinical response to probiotic treatment. We recruited 76 children with a median age of 7.1 years who suffered from moderate to severe AD. After a 2-week washout period, all patients were given Lactobacillus plantarum CJLP133 at a dosage of 1×1010 colony-forming units once a day for 12 weeks. We measured eosinophil counts in the peripheral blood, the proportion of CD4+CD25+Foxp3+ regulatory T (Treg) cells in CD4+ T cells, serum total immunoglobulin E (IgE) levels, and specific IgE against common allergens before the start of the treatment (T1) and at discontinuation (T2). Responders were defined as patients with at least a 30% reduction in the SCORing of AD (SCORAD) index after treatment. There were 36 responders and 40 non-responders after probiotic treatment. The median SCORAD was reduced from 29.5 (range 20.6-46.3) at T1 to 16.4 (range 6.3-30.8) at T2 in the responder group (P<0.001). In multivariable logistic regression analysis, a good clinical response was significantly associated with high total IgE levels (aOR 5.1, 95% CI 1.1-23.6), increased expression of transforming growth factor (TGF)-β (aOR 4.6, 95% CI 1.3-15.9), and a high proportion of Treg cells in CD4+ T cells (aOR 3.7, 95% CI 1.1-12.7) at T1. In the responder group, the proportion of Treg cells was significantly increased after 12 weeks of treatment (P=0.004), while TGF-β mRNA expression was decreased (P=0.017). Our results suggest that a subgroup of patients with a specific AD phenotype showing an immunologically active state (high total IgE, increased expression of TGF-β, high numbers of Treg cells) may benefit from probiotic treatment with L. plantarum CJLP133.

2018 ◽  
Vol 32 (6) ◽  
pp. 502-517 ◽  
Author(s):  
Nuray Bayar Muluk ◽  
Fazilet Altın ◽  
Cemal Cingi

Objectives Our intention was to review all material published to date regarding superantigens (SAgs) and allergy from an otorhinolaryngological viewpoint to understand this association more clearly. Methods We identified all materials published mentioning both SAg and allergic rhinitis (AR), chronic sinusitis, asthma, and atopic dermatitis (AD) that are indexed on PubMed, Google, or the ProQuest Central databases. Results Staphylococcus aureus is a significant bacterial pathogen in humans and has the ability to produce enterotoxins with superantigenic features. The inflammatory response in allergy seen in both B cell and T cell may be attributed to SAgs. Sufferers of both allergic asthma with rhinitis and AR alone produce serological evidence of immunoglobulin E formation to SAgs produced by S. aureus. Perennial AR sufferers carry S. aureus more frequently and the presence of the organism within the nasal cavity may exacerbate perennial AR. SAg produced by S. aureus potentially worsens the asthmatic inflammatory response within the airway and may lead to the airways becoming hyperresponsive, as well as possibly activating T cells if asthmatic control is poor. Staphylococcal SAgs potentially increase the risk of developing chronic rhinosinusitis with nasal polyposis, additionally being a marker for more severe disease. If SAgs bring about chronic inflammatory responses in the nose and sinuses, then T cells excreting interferon-gamma may be a crucial mediator. In allergic dermatitis, S. aureus could be a key player in exacerbation of the condition. Even in younger pediatric patients with allergic dermatitis, allergic hypersensitivity to SAgs is frequent and may be a factor explaining how severe the condition becomes. Conclusion Just as SAgs are known to feature in many allergic conditions, they play their part in AR, chronic rhinosinusitis, asthma, and AD. Further research is required before the relationship between SAgs and allergy can be adequately explained.


2019 ◽  
Vol 10 (1) ◽  
pp. 55-67 ◽  
Author(s):  
W.-G. Kim ◽  
G.-D. Kang ◽  
H.I. Kim ◽  
M.J. Han ◽  
D.-H. Kim

This study aimed to examine whether probiotics, which suppressed the differentiation of splenic T cells into type 2 helper T (Th2) cells and induced into regulatory T cells in vitro, alleviate allergic rhinitis (AR) and gut microbiota disturbance. We isolated Bifidobacterium longum IM55 and Lactobacillus plantarum IM76 from human faecal microbiota and kimchi, respectively, and examined their effects on ovalbumin (OVA)-induced AR and gut microbiota disturbance in mice. Treatment with IM55, IM76, or their probiotic mixture (PM) significantly reduced OVA-induced allergic nasal symptoms and blood immunoglobulin E (IgE) levels in mice. These also reduced OVA-induced interleukin (IL)-4 and IL-5 levels in nasal tissues and bronchoalveolar lavage fluid (BALF) but increased OVA-suppressed IL-10 levels. Treatment with IM55, IM76, or PM reduced OVA-induced increase in the populations of mast cells, eosinophils, and Th2 cells and increased OVA-suppressed population of regulatory T cells in the BALF. Treatment with IM55, IM76, or PM also inhibited OVA-induced expression of IL-5 in lung and colon tissues and restored OVA-disturbed composition of gut microbiota Proteobacteria, Bacteroidetes, and Actinobacteria. These results suggest that IM55 and IM67 can alleviate AR by restoring Th2/Treg imbalance and gut microbiota disturbance.


2020 ◽  
Vol 7 (1) ◽  
pp. 5-9
Author(s):  
Dr. Mayank Surana ◽  
Dr. Vineeta Pande ◽  
Dr. Sharad Agarkhedkar ◽  
Dr. Ajit Teegala

Allergy, is a clinical expression of soluble factors like IgE, histamine or eosinophils found in serum or plasma of such patients. The products that are responsible for allergy are called as Allergens. Allergens normally induce IgE production which leads to type 1 hypersensitivity response on subsequent exposure to the same allergen. The target organs are mostly nose, lung, skin and gastrointestinal tract. Atopy is also considered as a triad of Atopic dermatitis, allergic rhinitis and bronchial asthma. Raised serum IgE and AEC are proven indicators of allergic phenomenon. Various studies show relationship between serum Immunoglobulin E level and total eosinophil count in population suffering from allergic diseases. Serum total Immunoglobulin E, total eosinophil count and specific IgE are all helpful for the diagnosis and treatment of allergic diseases. Objectives: 1.To Evaluate Serum Total IgE level in Children with allergic diseases.2. To Evaluate Absolute Eosinophil Count (AEC) in children with allergic diseases.3. To Correlate Serum Total Immunoglobulin E Level and Absolute Eosinophil Count (AEC) with allergic diseases. Methodology: Cross sectional study with 100 children in the age group 2-12 years with nasopharyngeal allergies (like bronchial asthma and atopic rhinitis) and skin allergies (like atopic dermatitis, urticaria) ,eye allergies were enrolled and serum IgE levels and AEC levels was done. Results: In present study Absolute eosinophil count was raised in 58% of cases Serum IgE was raised in 54% of cases. In present study, of 58% cases with raised Absolute eosinophil count 81% (47 cases) showed raised serum IgE levels. Conclusion: Absolute eosinophil count and serum Total IgE has been considered as a significant marker of allergic state and can be used as a marker of allergic response in atopic individuals. Raised serum IgE and AEC are more in nasobronchial allergy as compare to other systemic allergies. The elevated level of serum Total IgE and Absolute Eosinophil Count both shows Significant Correlation thus can be considered as a dependable laboratory investigation in diagnosing and categorizing allergic diseases.


2002 ◽  
Vol 196 (2) ◽  
pp. 255-260 ◽  
Author(s):  
Helmut Jonuleit ◽  
Edgar Schmitt ◽  
Hacer Kakirman ◽  
Michael Stassen ◽  
Jürgen Knop ◽  
...  

Regulatory CD4+CD25+ T cells (Treg) are mandatory for maintaining immunologic self-tolerance. We demonstrate that the cell-cell contact–mediated suppression of conventional CD4+ T cells by human CD25+ Treg cells is fixation resistant, independent from membrane-bound TGF-β but requires activation and protein synthesis of CD25+ Treg cells. Coactivation of CD25+ Treg cells with Treg cell–depleted CD4+ T cells results in anergized CD4+ T cells that in turn inhibit the activation of conventional, freshly isolated CD4+ T helper (Th) cells. This infectious suppressive activity, transferred from CD25+ Treg cells via cell contact, is cell contact–independent and partially mediated by soluble transforming growth factor (TGF)-β. The induction of suppressive properties in conventional CD4+ Th cells represents a mechanism underlying the phenomenon of infectious tolerance. This explains previously published conflicting data on the role of TGF-β in CD25+ Treg cell–induced immunosuppression.


2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Masanori Abe ◽  
Yoichi Hiasa ◽  
Morikazu Onji

Many autoimmune diseases are driven by self-reactive T helper (Th) cells. A new population of effector CD4+T cells characterized by the secretion of interleukin (IL)-17, referred to as Th17 cells, has been demonstrated to be phenotypically, functionally, and developmentally distinct from Th1 and Th2 cells. Because the liver is known to be an important source of transforming growth factor-βand IL-6, which are cytokines that are crucial for Th17 differentiation, it is very likely that Th17 cells contribute to liver inflammation and autoimmunity. In contrast, another distinct subset of T cells, regulatory T cells (Treg), downregulate immune responses and play an important role in maintaining self-tolerance. In addition, there is a reciprocal relationship between Th17 cells and Tregs, in development and effector functions, and the balance between Th17 and Treg cells can affect the outcome of immune responses, particularly in autoimmune diseases. In this review, we will focus on the latest investigative findings related to Th17 cells in autoimmune liver disease.


Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3920-3920
Author(s):  
Yun Ling ◽  
Xiangshan Cao ◽  
Ziqiang Yu ◽  
Changgeng Ruan

Abstract Immune thrombocytopenic purpura (ITP) is an autoimmune disorder and high-dose dexamethasone (HD-DXM) has been used as a first-line therapy for patients with ITP. However, little is known about the role of CD4+CD25 + regulatory T (Treg) cells, interleukin-10 (IL-10) and transforming growth factor-β1 (TGF-β1) in the pathogenesis of chronic ITP and the effects of HD-DXM on them contained Treg cells, IL-10 and TGF-β1. In this study, we investigated the expressions of Treg cells, IL-10 and TGF-β1 in 26 untreated adult patients with chronic ITP. All patients had thrombocytopenia (platelet count &lt;50 × 109/L) for more than 6 months. We also observed short time changes of Treg cells, IL-10 and TGF-β1 after treatment with HD-DXM in these patients. The results showed that a good initial response to HD-DXM occurred in 24 of the 26 patients with chronic ITP (92.3%): the mean platelet count was (84.9±30.4)×109/L [range, (20∼150) ×109/L] one week after the initiation of treatment. The proportion of CD4+CD25+ T cells in the peripheral blood of patients with chronic ITP was significantly higher than that in normal controls(P&lt;0.001); there was no significant difference in the percentage of CD4+CD25high T cells between patients and controls ( P=0.317); but the number of CD4+ FOXP3+ T cells in patients was significantly lower than that in controls (P&lt;0.001). After 4-days treatment with HD-DXM, the numbers of CD4+ CD25+ T cells (P&lt;0.001), CD4+CD25high T cells ( P&lt;0.001), and CD4+FOXP3+ T cells ( P&lt;0.001) in patients were all significantly increased. In the serum of chronic ITP patients, the expression level of TGF-β1 was lower than that of healthy controls (P&lt;0.0001) and HD-DXM could significantly increase it; there was no significant difference in the expression level of IL-10 between patients and controls ( P&gt;0.05) and there was no remarkable change of IL-10 in patients after HD-DXM treatment (P&gt;0.05). The mRNA levels of Foxp3 and TGF-β1 gene in patients were lower than those of controls (P&lt;0.05 and P&lt;0.05); HD-DXM administration significantly increased the expressions of Foxp3 and TGF-β1 gene(P&lt;0.05 and P&lt;0.0001), which were even higher than those of controls(P&lt;0.05 and P&lt;0.05); There was a positive correlation between the Foxp3 mRNA expression and TGF-β1 after treatment with HD-DXM (r =0.403, P=0.041). These results suggest that Foxp3 and TGF-β1 gene are deficient in chronic ITP and the immunosuppressive therapy of glucocorticoids could improve the expression levels of these genes.


2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Jiangping Song ◽  
Jie Huang ◽  
Xiao Chen ◽  
Xiao Teng ◽  
Zhizhao Song ◽  
...  

Abstract To inhibit the immune inflammation in the allografts can be beneficial to organ transplantation. This study aims to induce the donor antigen specific regulatory T cells (Treg cell) inhibit the immune inflammation in the allograft heart. In this study, peripheral exosomes were purified from the mouse serum. A heart transplantation mouse model was developed. The immune inflammation of the allograft heart was assessed by histology and flow cytometry. The results showed that the donor antigen-specific T helper (Th)2 pattern inflammation was observed in the allograft hearts; the inflammation was inhibited by immunizing the recipient mice with the donor-derived exosomes. Purified peripheral exosomes contained integrin MMP1a; the latter induced CD4+ T cells to express Fork head protein-3 and transforming growth factor (TGF)-β via inhibiting the Th2 transcription factor, GATA binding protein 3, in CD4+ T cells. Administration with the donor-derived exosomes significantly prolonged the allograft heart survival. We conclude that the donor-derived peripheral exosomes have the capacity to inhibit the immune inflammation in the allograft heart via inducing specific Treg cells, implicating that administration with the donor-derived exosomes may be beneficial to cardiac transplantation.


2010 ◽  
Vol 78 (10) ◽  
pp. 4392-4401 ◽  
Author(s):  
Maria Carolina Ferreira ◽  
Rômulo Tadeu Dias de Oliveira ◽  
Rosiane Maria da Silva ◽  
Maria Heloisa Souza Lima Blotta ◽  
Ronei Luciano Mamoni

ABSTRACT Patients with paracoccidioidomycosis (PCM) exhibit a suppression of the cellular immune response characterized by negative delayed-type hypersensitivity (DTH) to Paracoccidioides brasiliensis antigens, the apoptosis of lymphocytes, and high levels of expression of cytotoxic-T-lymphocyte-associated antigen 4 (CTLA-4), interleukin-10 (IL-10), and transforming growth factor β (TGF-β). The aim of this study was to investigate whether and how regulatory T cells (Treg cells) are involved in this immunosuppression by analyzing the number, phenotype, and activity of these cells in patients with active disease (AD group) and patients who had received treatment (TD group). Our results showed that the AD patients had more Treg cells than the TD patients or controls (C group) and also had elevated levels of expression of regulatory markers (glucocorticoid-induced tumor necrosis factor [TNF] receptor-related protein [GITR], CTLA-4, CD95L, LAP-1, and CD38). An analysis of regulatory activity showed that Treg cells from the AD group had greater activity than did cells from the other groups and that cell-cell contact is mandatory for this activity in the C group but was only partially involved in the regulatory activity of cells from AD patients. The addition of anti-IL-10 and anti-TGF-β neutralizing antibodies to the cultures showed that the production of cytokines may be another mechanism used by Treg cells. In conclusion, the elevated numbers of these cells with an increased regulatory phenotype and strong suppressive activity suggest a potential role for them in the immunosuppression characteristic of paracoccidioidomycosis. In addition, our results indicate that while Treg cells act by cell-cell contact, cytokine production also plays an important role.


Biomedicines ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 461
Author(s):  
Jorge Gallego-Valle ◽  
Sergio Gil-Manso ◽  
Ana Pita ◽  
Esther Bernaldo-de-Quirós ◽  
Rocío López-Esteban ◽  
...  

Regulatory T cells (Tregs), which are characterized by the expression of the transcription factor forkhead box P3 (FOXP3), are the main immune cells that induce tolerance and are regulators of immune homeostasis. Natural Treg cells (nTregs), described as CD4+CD25+FOXP3+, are generated in the thymus via activation and cytokine signaling. Transforming growth factor beta type 1 (TGF-β1) is pivotal to the generation of the nTreg lineage, its maintenance in the thymus, and to generating induced Treg cells (iTregs) in the periphery or in vitro arising from conventional T cells (Tconvs). Here, we tested whether TGF-β1 treatment, associated with interleukin-2 (IL-2) and CD3/CD28 stimulation, could generate functional Treg-like cells from human thymocytes in vitro, as it does from Tconvs. Additionally, we genetically manipulated the cells for ectopic FOXP3 expression, along with the TGF-β1 treatment. We demonstrated that TGF-β1 and ectopic FOXP3, combined with IL-2 and through CD3/CD28 activation, transformed human thymocytes into cells that expressed high levels of Treg-associated markers. However, these cells also presented a lack of homogeneous suppressive function and an unstable proinflammatory cytokine profile. Therefore, thymocyte-derived cells, activated with the same stimuli as Tconvs, were not an appropriate alternative for inducing cells with a Treg-like phenotype and function.


Sign in / Sign up

Export Citation Format

Share Document