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Additional file 1: Table S1. Systematic search strategy. Table S2. Systematic search on IgE autoantibodies in patients with atopic dermatitis. AD: atopic dermatitis, RC: rhino conjunctivitis, NA: nonatopic, HC: healthy controls without allergic symptoms, PS: psoriasis, CA: contact allergy, UA: urticaria. Table S3. Autoreactive T cells in patients with atopic dermatitis. AD: atopic dermatitis, RC: rhinoconjunctivitis, HC: healthy controls, NA: non-atopic, CD: chronic dermatoses, PS: psoriasis, ns: non-sensitized, ABPA: allergic bronchopulmonary aspergillosis. * median.

Diabetes mellitus is a group of disorders characterized by prolonged high levels of circulating blood glucose. Type 1 diabetes is caused by decreased insulin production in the pancreas whereas type 2 diabetes may develop due to obesity and lack of exercise; it begins with insulin resistance whereby cells fail to respond properly to insulin and it may also progress to decreased insulin levels. The brain is an important target for insulin, and there is great interest in understanding how diabetes affects the brain. In addition to the direct effects of insulin on the brain, diabetes may also impact the brain through modulation of the inflammatory system. Here we investigate how perturbation of circulating insulin levels affects the expression of Hes3, a transcription factor expressed in neural stem and progenitor cells that is involved in tissue regeneration. Our data show that streptozotocin-induced β-cell damage, high fat diet, as well as metformin, a common type 2 diabetes medication, regulate Hes3 levels in the brain. This work suggests that Hes3 is a valuable biomarker helping to monitor the state of endogenous neural stem and progenitor cells in the context of diabetes mellitus.

Ze339, an herbal extract from Petasites hybridus leaves is effective in treatment of allergic rhinitis by inhibition of a local production of IL-8 and eicosanoid LTB4 in allergen-challenged patients. However, the mechanism of action and anti-inflammatory potential in virally induced exacerbation of the upper airways is unknown. This study investigates the anti-inflammatory mechanisms of Ze339 on primary human nasal epithelial cells (HNECs) upon viral, bacterial and pro-inflammatory triggers. To investigate the influence of viral and bacterial infections on the airways, HNECs were stimulated with viral mimics, bacterial toll-like-receptor (TLR)-ligands or cytokines, in presence or absence of Ze339. The study uncovers Ze339 modulated changes in pro-inflammatory mediators and decreased neutrophil chemotaxis as well as a reduction of the nuclear translocation and phosphorylation of STAT molecules. Taken together, this study suggests that phyto drug Ze339 specifically targets STAT-signalling pathways in HNECs and has high potential as a broad anti-inflammatory drug that exceeds current indication.

Additional file 1: Appendix S1. Search strategy.

Hintergrund: Ze339 (IG-RD-001) ist ein CO2-Extrakt von Petasites hybridus. Seine Wirksamkeit bei allergischer Rhinitis wurde bereits in kontrollierten randomisierten klinischen Studien untersucht. In vitro zeigte sich eine verminderte Mediatorfreisetzung durch Eosinophile und eine Hemmung der Leukotriensynthese.[for full text, please go to the a.m. URL], 81. Jahresversammlung der Deutschen Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie

Interleukin 22 (IL-22) is а newly-described Т helper cytokine which has been implicated in tissue regenerative processes in the gut and skin. Allergic asthma results from exposure to otherwise harmless environmental inhaled allergens that trigger Th2 Т Iymphocyte-driven IgE-аssосiаtеd immune responses in atopic individuals that contribute to airway inflammation and reversible airflow obstruction. In the long-term, this aberrant immune response is believed to increase in complexity and contribute to the permanent changes in the airways, including tissue remodelling and associated irreversible airway obstruction. In view of the known effects of IL-22 in wound healing, the overall aim of this research was to establish whether IL-22 is present in allergy and allergic asthma and to understand the influence of IL-22 on structural cells of the airway, with particular emphasis оп tissue remodelling. We, therefore, explored the presence of IL-22 and its receptors during allergen-induced late responses in the bronchi and skin and measured IL-22 production and its regulation in peripheral blood mononuclear cells (PBMCs), Т cell lines and clones derived from asthmatic bronchial muсоsa. IL-22 was increased in bгonchoalveolaг lavage after allergen inhalation in asthmatics but not in control subjects. While we were unable to reliably immunostain IL-22, its receptors were present within the cutaneous connective tissue and co-Iocalised with HSP-47, а marker of early fibrobIasts. In PBMCs, IL-22 increased after allergen stimulation whereas there was nо difference between atopics and control subjects. In Т cell lines derived from asthmatic bronchial mucosa, IL-22 was mainly found in СD4+ Т helper cells of Th1 and Th22 origin. IL-22 receptors were expressed by cultured bronchial epithelial cells, smooth muscle cells and pulmonary fibroblasts and were increased in expression in the presence of interferon-γ (IFN-γ). IL-22 was able to accelerate wound closure of bronchial epithelial cells independent of effects on cellular proliferation. Thus, IL-22 appears to be а Th1-related cytokine that may have а dual role in airway inflammation and repair.

Specific immunotherapy (SIT) represents the only curative treatment of allergy and is, therefore, of particular interest for immunological and pharmacological research. The current understanding of immunological mechanisms underlying SIT focuses on regulatory T cells (T regs), which balance Th1 and Th2 effector functions. This ensures that allergens are recognized, but tolerated by the immune system. There is clear evidence that SIT restores the disturbed balance of T regs and effector cells in allergic patients. Current efforts are focused to improve SIT regimens to make them more applicable in atopy and asthma. The current review provides an overview on the mechanisms of SIT and possible adjuvant treatment strategies on the background of the T reg concept.