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Asthma was previously defined as an allergic Th2-mediated inflammatory immune disorder. Recently, this paradigm has been challenged since not all pathological changes observed in the asthmatic airways are adequately explained simply as a result of Th2-mediated processes. Contemporary thought holds that asthma is a complex immune disorder involving innate as well as adaptive immune responses, with the clinical heterogeneity of asthma perhaps a result of the different relative contribution of these two systems to the disease.

Epidemiological studies show that exposure to certain environmental substances is strongly associated with the risk of developing asthma. The airway epithelium is first barrier to interact with, and respond to, environmental agents (pollution, viral infection, allergens) suggesting that it is a key player in the pathology of asthma. Epithelial cells play a key role in the regulation of tissue homeostasis by the modulation of numerous molecules, from antioxidants and lipid mediators to growth factors, cytokines and chemokines. Additionally, the epithelium is also able to suppress mechanisms involved in e.g. inflammation in order to maintain homeostasis. An intrinsic alteration or defect in these regulation mechanisms compromises the epithelial barrier, and therefore the barrier may be more prone to environmental substances and thus more likely to exhibit an asthmatic phenotype. In support of this, polymorphisms in a number of genes that are expressed in the bronchial epithelium have been linked to asthma susceptibility, while environmental factors may affect epigenetic mechanisms that can alter epithelial function and response to environmental insults.

A detailed understanding of the regulatory role of the airway epithelium is required in order to develop new therapeutic strategies for asthma that not only address the symptoms but also the underlining pathogenic mechanism(s) and prevent airway remodelling. This article is protected by copyright. All rights reserved.

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Toll-like receptors (TLRs) are pattern recognition receptors crucial for the innate and adaptive immune response to pathogen-associated molecular patterns (PAMPs). TLR stimulation via microbial products activates antigen-presenting cells, influences the function of T regulatory cells (Treg), determines the Th1/Th2 balance and Th17 cell differentiation, and controls cytokine production in mast cells and activation of eosinophils.

The role of TLR receptors in pathogenesis of allergic diseases results from the biological function that they play in activation and regulation of the immune response. However, the exact role still remains a controversial area. Whereas numerous epidemiological studies mainly indicate a protective effect of microbial exposure, experiments show that innate immune stimulation via TLRs may be involved in both development of and protection against allergic diseases. Timing, dose, site and intensity of exposure to environmental factors and host genetic predisposition are clearly crucial to understanding the interaction between innate immune stimulation and allergy development.Furthermore, extensive clinical trials suggest that ligands for TLRs provide new therapeutic targets for protection against and treatment of asthma and allergic rhinitis.

The aim of this review is to summarize the current knowledge about the role of TLRs in pathogenesis of allergic diseases. We will further discuss how we can reconcile inconsistencies in the results of existing studies and review information on the potential use of ligands for TLRs in allergy prevention and therapy.

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Skin prick tests are widely used to determine sensitivity in allergic diseases. There is limited information about the natural history of skin sensitization tests and factors that affect them.

It was aimed to determine the changes in skin test results and the factors affecting the reactivity of skin tests after a period of approximately four years in children with allergic disease.

Methods: SPT of 170 patients among 2485 children with asthma and/or allergic rhinitis and/or atopic dermatitis, who underwent SPT between 2005 and 2007, were repeated after an interval of at least 3 years.

Results: The mean age was 10.7 ± 3.1 (5-18) years and 70% of the patients were male. In total 66 (39.0% of the study population) had a different skin tests result in follow-up. Alterations: loss of sensitivity in 18 (11%) patients, the formation of a new sensitivity in 37 (22%) patients, and 11 (6%) both gained and lost sensitization. The presence of atopy in the family, the presence of allergic rhinitis and IgE elevation significantly predicted the incidence of new sensitization. The presence of sensitization to multiple allergens significantly predicted the incidence of loss of sensitization.

Conclusions: It is found that there was an alteration of sensitization in 4/10 children at the end of the average 4-year period. The presence of family atopy, the presence of allergic rhinitis and serum total IgE elevation were risk factors for the development of new sensitization. On the other hand sensitization to multiple allergens was risk factors for the loss of sensitization.

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Periostin, an extracellular matrix protein belonging to the fasciclin family, has been shown to play a critical role in the process of remodeling during tissue/organ development or repair. Periostin functions as a matricellular protein in cell activation by binding to their receptors on cell surface, thereby exerting its biological activities.

After we found that periostin is a downstream molecule of interleukin (IL)-4 and IL-13, signature cytokines of type 2 immune responses, we showed that periostin is a component of subepithelial fibrosis in bronchial asthma, the first formal proof that periostin is involved in allergic inflammation. Subsequently, a great deal of evidence has accumulated demonstrating the significance of periostin in allergic inflammation. It is of note that in skin tissues, periostin is critical for amplification and persistence of allergic inflammation by communicating between fibroblasts and keratinocytes. Furthermore, periostin has been applied to development of novel diagnostics or therapeutic agents for allergic diseases. Serum periostin can reflect local production of periostin in inflamed lesions induced by Th2-type immune responses and also can predict the efficacy of Th2 antagonists against bronchial asthma. Blocking the interaction between periostin and its receptor, αv integrin, or down-regulating the periostin expression shows improvement of periostin-induced inflammation in mouse models or in in vitro systems.

It is hoped that diagnostics or therapeutic agents targeting periostin will be of practical use in the near future.

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