IL‐17 producing T cells correlate with polysensitization but not with bronchial hyperresponsiveness in patients with allergic rhinitis

Tsvetkova-Vicheva, Vanya; Gecheva, S.; Komsa-Penkova, Regina; Velkova, A; Lukanov, Tzvetan

doi:10.1186/2045-7022-4-3

Cited by 13 publications

(16 citation statements)

References 14 publications

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“…A human population of Th17 cells that express CD39 also are resistant to the effects of adenosine as a consequence of low expression of A 2A Rs (30). Moreover, IL-17 may be particularly important for controlling airway hyperresponsiveness (43). The findings also demonstrate that CGS administered at a dose of 100 ng·kg Ϫ1 ·min Ϫ1 does not have significant direct bronchodilator effects.…”

Section: Myeloid Cells As Targets Ofmentioning

confidence: 90%

Adenosine influences myeloid cells to inhibit aeroallergen sensitization

Pei

Linden

2016

American Journal of Physiology-Lung Cellular and Molecular Phys

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Agonists of adenosine A2A receptors (A2ARs) suppress the activation of most immune cells and reduce acute inflammatory responses. Asthma is characterized by sensitization in response to initial allergen exposure and by airway hyperreactivity in response to allergen rechallenge. We sought to determine if A2AR activation with CGS-21680 (CGS) is more effective when CGS is administered during sensitization or rechallenge. C57BL/6 wild-type mice and Adora2a(f/f)LysMCre(+/-) mice, which lack A2ARs on myeloid cells, were sensitized with intranasal ovalbumin (OVA) and LPS. Airway sensitization was characterized by a rapid increase in numbers of IL-6(+) and IL-12(+) macrophages and dendritic cells in lungs. A2AR activation with CGS (0.1 μg·kg(-1)·min(-1) sc) only during sensitization reduced numbers of IL-6(+) and IL-12(+) myeloid cells in the lungs and reversed the effects of OVA rechallenge to increase airway hyperresponsiveness to methacholine. CGS treatment during sensitization also reduced the expansion of lung T helper (Th1 and Th17) cells and increased expansion of regulatory T cells in response to OVA rechallenge. Most of the effects of CGS administered during sensitization were eliminated by myeloid-selective A2AR deletion. Administration of CGS only during OVA rechallenge failed to reduce airway hyperresponsiveness. We conclude that myeloid cells are key targets of adenosine during sensitization and indirectly modify T cell polarization. The results suggest that a clinically useful strategy might be to use A2AR agonists to inhibit sensitization to new aeroallergens. We speculate that adenosine production by macrophages engulfing bacteria contributes to the curious suppression of sensitization in response to early-life infections.

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Section: Myeloid Cells As Targets Ofmentioning

confidence: 90%

Adenosine influences myeloid cells to inhibit aeroallergen sensitization

Pei

Linden

2016

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…It has been proved that goblet cell hyperplasia, mast cell infiltration, Th-2, Th-9 and Th-17 polarization are recognized as important features of AR 3 5 22 23 . In the present study, significantly increased goblet cell hyperplasia, mast cell infiltration, IL-4, IL-9 and IL-17 levels were found in AR mice compared with normal control mice, which is consistent with previous reports 3 5 22 23 . In addition, MUC5AC and tryptase mRNA levels were significantly upregulated in AR mice compared with normal control mice, further confirming that goblet cell hyperplasia and mast cell infiltration are involved in the pathogenesis of AR.…”

Section: Discussionmentioning

confidence: 99%

Lentiviral shRNA against KCa3.1 inhibits allergic response in allergic rhinitis and suppresses mast cell activity via PI3K/AKT signaling pathway

Lin

Zheng

et al. 2015

Sci Rep

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Calcium-activated potassium ion channel-3.1 (KCa3.1) plays a pivotal role in the potassium-calcium exchange involved in atopy. This study aimed to explore the impact of lentiviral-mediated shRNA silencing KCa3.1 on allergic response in a murine allergic rhinitis (AR) model. The BALB/c mice were divided into four groups: untreated AR group, negative control AR group, lentiviral KCa3.1-shRNA treated AR group and normal control group. Concentrations of ovalbumin (OVA)-specific IgE, histamine and leukotrienes C4 (LTC4) in serum, and IL-4, IL-9 and IL-17 in nasal lavage fluid (NLF) were analyzed. Goblet cells and mast cells were counted. KCa3.1 positive cells were counted after immunolabelling by immunofluorescence method. KCa3.1, Mucin 5AC (MUC5AC), and tryptase mRNA levels were determined using real-time polymerase chain reaction. Furthermore, P815 cell line was used to explore the role and mechanism of lentiviral KCa3.1-shRNA on mast cells. The results showed that LV-KCa3.1-shRNA intervention effectively attenuated allergic responses in LV-KCa3.1-shRNA treated mice. LV-KCa3.1-shRNA intervention effectively suppressed KCa3.1 levels and phosphorylation of AKT in P815 cells, leading to the downregulation of tryptase, IL-6 and IL-8 levels. LV-KCa3.1-shRNA intervention effectively attenuated the allergic responses in AR and suppressed mast cell activity by inhibiting PI3K/AKT signaling pathway.

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“…However, in most of these studies, patients allergic to perennial allergens [27, 28] or sensitive to seasonal and perennial allergens were involved [29]. Another study describes the influence of perennial allergen challenge by nebulization on Th 17 cells [30], however, less is known about changes over time caused by natural seasonal allergen exposure.…”

Section: Discussionmentioning

confidence: 99%

“…Another study describes the influence of perennial allergen challenge by nebulization on Th 17 cells [30], however, less is known about changes over time caused by natural seasonal allergen exposure. It was shown that the percentage of IL-17A-producing CD4+ T cells may also depend on polysensitization of the patients and on patient’s sex [29]. Although an increased serum IL-17 level was observed in patients sensitive to perennial allergens, pollen allergens did not cause significant changes [29].…”

Section: Discussionmentioning

confidence: 99%

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Th17 responses are not altered by natural exposure to seasonal allergens in pollen-sensitive patients

Schramm

Jasiewicz-Honkisz

Osmenda

et al. 2016

Allergy Asthma Clin Immunol

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BackgroundAllergic rhinitis affects 10–30 % of the global population and this number is likely to increase in the forthcoming years. Moreover, it commonly co-exists with allergic asthma as a chronic allergic respiratory syndrome. While the involvement of Th2 cells in allergy is well understood, alterations of pro-inflammatory Th17 responses remain poorly characterized. The aim of our study was to determine whether natural seasonal allergen exposure causes changes in T cell subset characteristics in patients with allergic rhinitis and asthma.MethodsSixteen patients with allergic rhinitis/atopic asthma (9M, 7F; age 31.8 ± 12.1) and 16 healthy controls were recruited into the study (9M, 7F; age 31.2 ± 5.3). Blood samples were collected from the patients 1–3 months before pollen season (visit 1), within 7 days of the appearance of pollen/initiation of allergic symptoms (visit 2) and 2 weeks after visit 2 following the introduction of symptomatic treatment with antihistamines (visit 3). Flow cytometry was used to assess major T cell subsets (naïve, central memory, effector memory and CD45RA+ effector) and key T cell cytokine production (IFNγ, IL-17A, TNF and IL-4) using intracellular staining. Data were analyzed using repeated measures ANOVA and paired t test.ResultsAs expected, an increase in the percentage of IL‐4+ CD4+ cells was observed during natural pollen exposure in patients with allergic respiratory syndrome. No significant changes were observed in the production of other cytokines, including Th17 cells, which tended to be lower than in the control population but unchanged during pollen exposure. Introduction of antihistamine treatment led to only moderate changes in cytokine production from CD4 and CD8 T cells. Selective changes in CD8+ T cells were observed during natural pollen exposure including a decrease in transient cells (with features of CD45RA+ and CD45RO+ cells) and a decrease in the percentage of central memory cells in the peripheral circulation. Within the CD4 cell group the total percentage of CD45RA positive CD4 cells was increased during pollen exposure.ConclusionsTh1 and Th17 responses are not altered during pollen season but allergen exposure affects T cell activation and memory cell status in patients with allergic respiratory syndrome.Electronic supplementary materialThe online version of this article (doi:10.1186/s13223-016-0157-6) contains supplementary material, which is available to authorized users.

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IL‐17 producing T cells correlate with polysensitization but not with bronchial hyperresponsiveness in patients with allergic rhinitis

Cited by 13 publications

References 14 publications

Adenosine influences myeloid cells to inhibit aeroallergen sensitization

Adenosine influences myeloid cells to inhibit aeroallergen sensitization

Lentiviral shRNA against KCa3.1 inhibits allergic response in allergic rhinitis and suppresses mast cell activity via PI3K/AKT signaling pathway

Th17 responses are not altered by natural exposure to seasonal allergens in pollen-sensitive patients

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