Immune cells were recognized to play a central role in pathophysiological concepts such as asthma. Recently, it is worth noting that role of airway epithelial cell for pathogenesis or exacerbation of allergic diseases. Epithelial cells make up not only the first line of defense against inhaled environmental factors, such as pathogens, allergens, and pollutants, but not act function in the regulation of immune responses through the production of cytokines and chemokines and via interaction with cells of immune systems. There are increasing evidences that epithelial cells are recognized as a main source of Th2 type inflammation. It is suggest that exposed of inhaled allergen against epithelial cells may result in part from decreased epithelial barrier and innate immune responses including TSLP, IL-25, IL-33, subsequent the development and/or exacerbation of allergic diseases. IL-25 (also known as IL-17E) is a member of the IL-17 family of cytokines. IL-25 acts in promoting a Th2-type immune response and affects in recently identified type 2 innate lymphoid cells. This review summarizes the current knowledge regarding role of IL-25 and the mechanism of IL-25 production outside airway epithelial cells.

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Allergic rhinitis is a significant global health care problem. Double strand RNAs (dsRNA) degrade mRNAs in a specific manner and inhibit expression of gene highly. This phenomenon is an endogenous cellular defense mechanism to eliminate viruses that invade the cell and transposable elements in the genome. Andrew Fire and Creig Mello received the 2006 Nobel Prize in Medicine for this finding. In order to induce RNA interference, long pieces of 200-800 base pairs of dsRNA had been used. However, long dsRNAs are degraded intracellularly to 21-23 bp RNAs and this short RNAs can degrade the target mRNA. These small pieces of RNA, called small interfering RNA (siRNA), can block gene expression in mammalian cells without triggering the nonspecific panic response. Sequence-specific siRNA is able to target and cleave complementary mRNA. siRNA has very high specificity and differences of a few base pairs can eliminate the effect of siRNA completely. Here we discuss the potential of siRNA to attenuate allergic rhinitis.

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Eosinophils are key players in Th2 pathologies such as asthma. However, their exact contribution to airway inflammation remains controversial. To investigate whether eosinophil can promote airway inflammation, adoptive transfers of eosinophils from IL-5 transgenic mice were performed into the recipient mice. Adoptively transferred activated eosinophils, but not naïve eosinophils induced airway inflammation in the absence of lymphocytes. Moreover, we reported that IFN-γ expression was significantly increased in the lung of eosinophil-induced airway inflammation, and eosinophil-derived IFN-γ induced airway hyperresponsiveness and lung inflammation. These results evidence the important and previously unsuspected contribution of eosinophils to lung inflammation, independently of lymphocytes, through the production of IFN-γ. Thus, our results suggest that eosinophil-derived IFN-γ is an important mediator of lung inflammation. Here, we examine the essential and functional role of eosinophil in the airway inflammation, and discuss the therapeutic strategies based on classical Th1/Th2 theory for eosinophil-associated diseases.

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Retraction notice

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