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Airway Allergy and Viral Infection

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Airway Allergy and Viral Infection Review article Airway allergy and viral infection Pongsakorn Tantilipikorn1 and Prasert Auewarakul2 Summary CD = Cluster of differentiation There are complex interactions between FoxP3 = Forkhead box P3 airway allergy and viral infection. Available IDO = Indoleamine 2,3-deoxygenase evidence suggests that viral respiratory infection TLR = Toll-like receptor can initiate, maintain and activate exacerbation TSLP = Thymic stromal lymphopoietin of allergic conditions in respiratory tract. Innate DC-SIGN = Dendritic cell-specific inter- and inflammatory responses to acute viral cellular adhesion molecule-3- infection play important roles in its relationship grabbing non-integrin to allergic reactions. On the other hand, biased ADAM33 = A disintegrin and metallo- immune responses toward Th2 caused by an proteinase – 33 allergic reaction may make the immune response EGF = Epidermal growth factor ineffective in combating viral infection. It was MMP = Matrix metalloproteinase previously shown that allergy can increase the PAMP = Pathogen-associated molecular expression level of rhinovirus receptors on pattern mucosal epithelial cells. This suggests that airway RIG1 = Retinoid-inducible gene 1 allergy may increase the risk of rhinovirus MDA5 = Melanoma differentiation- infection. We have recently shown that allergy associated gene 5 may also increase the expression level of ICAM = Intercellular adhesion molecule influenza virus receptors. This suggests that GC = Glucocorticoids airway allergy and viral infection may have a reciprocal interaction. The effect of allergy on the risk and outcome of viral infection needs to be Allergic inflammation of the airway further confirmed in clinical studies and its Development of allergic inflammation potential implication for clinical practice should Allergic inflammation is caused by IgE-mediated be considered. (Asian Pac J Allergy Immunol allergy. It can be divided into two phases. The first 2011;29:113-9) phase is the sensitization phase. In this phase, an Key words: airway, allergy, virus, influenza, allergen absorbed through airway epithelium is inflammation, glucocorticoids, viral infection, viral taken up by antigen-presenting cells (APC) and after receptor, asthma, Th2, airway epithelium internal processing a portion of the antigen is presented to T cells. In individuals whose signals from APC cause differentiation of T-helper 2 cell Abbreviations (Th2), production of cytokines, especially Th = T helper interleukin (IL) 4 and IL13, will drive a B cell class- APC = Antigen-presenting cell switch leading to the production of allergen-specific IL = Interleukin IgE (sIgE)1. The sIgE will bind to the surface of sIgE = Specific immunoglobulin E mast cells and becomes “sensitized”. The particular T reg = Regulatory T cell person who has sensitized mast cell and usually has TGF-β = Transforming growth factor beta a hereditary background is an “atopic” person. iTreg = Inducible regulatory T cell The second phase is called the re-exposure phase. In this phase, the sensitized mast cells encounter the same allergen which is specific to the 1 IgE bound on their surfaces. The mast cells become From the Departments of Oto-Rhino-Laryngology 2 Microbiology, activated and release several inflammatory Faculty of Medicine Siriraj Hospital mediators such as histamine and proteases. When Corresponding author: Prasert Auewarakul allergic inflammation occurs, the clinical E-mail: [email protected] Submitted date: 20/1/2011 manifestation can be recognized as allergic rhinitis, 113 Asian Pac J Allergy Immunol 2011;29:113-9 allergic asthma or dermatitis depending on the organ properties of allergens that may be involved in involved, which is called the “shock” organ. allergic sensitization include the ability to bind to or In normal individuals, exposure to common and induce signaling through innate receptors such as non-harmful antigens results in immune tolerance, Toll-like receptor (TLR) and DC-SIGN and the which prevents unnecessary and detrimental enzymatic activity that causes oxidative stress, immunological and inflammatory responses2. which can activate epithelial cells and DCs9. Tolerance is not merely a lack of immune response; Airway epithelium and its interaction to various on the contrary, it is a specific immunological microbes response that is mediated by T cells. Regulatory T Airway epithelium was initially considered to cells (Treg) expressing Foxp3 play a pivotal role in function solely as a physical barrier to a wide the induction of tolerance3. Induction of the Foxp3+ variety of environmental stimuli , such as allergens, peripheral induced Treg (iTreg) requires TGF-β4, infection (particularly virus) , airborne pollutants which is produced by various cell types including and drug11. Recently more understanding of a Th3 CD4+ T cells. In the presence of TGF-β, balance between the functions of innate immune antigen presenting cells, such as B cells and cells and the induction of adaptive immunity has dendritic cells (DCs), can present antigens to naïve been proposed12, 13. Airway epithelium can respond T cells and induce antigen-specific iTreg resulting in to various stimuli, such as allergens, infections immune tolerance5. The CD4+CD25+FoxP3+ iTreg (particularly viruses) and airborne pollutants. cells produce IL-10, which is an anti-inflammatory Respiratory epithelial cells play a crucial role in the cytokine6. initiation of innate immune responses by producing Allergic sensitization takes place by a failure in various cytokines. Epithelial-derived cytokines that tolerance induction or maintenance resulting in the have been implicated in initiating Th2 responses and induction of a Th2 type response. The Th2-produced allergic sensitization include TSLP, IL-33, and IL- IL4 and IL13 are the most important cytokines for 25. TSLP is an epithelial cell-derived cytokine that the pathogenesis of allergic asthma. IL4 is important can activate myeloid DC and the TSLP-activated for IgE production and eosinophilic inflammation, DC promotes Th2 response. IL-33 is produced by while IL13 is responsible for the changes in lung epithelial cells, fibroblasts, and endothelial cells. It tissue, such as bronchial hyper-responsiveness, is released when the cells become necrotic and binds overproduction of mucus, thickening of smooth to ST2 (IL-1RL1), a receptor expressed on Th2 muscle and subepithelial fibrosis7. cells, to activate the Th2 response. IL-25 is Other factors known to influence tolerance produced by Th2 cells, mast cells, alveolar induction include the tryptophan-catabolizing macrophages and epithelial cells with allergic enzyme indoleamine 2,3-deoxygenase (IDO). The reactions. It stimulates the production of Th2-type observation that IDO and other enzymes that cytokines and can induce allergic inflammation. 14, 15 catabolize essential amino acids are upregulated More importantly, a new model for asthma under conditions stimulating tolerance suggests that pathogenesis has recently been proposed, in which local immune responses may be tightly controlled epithelial and mesenchymal tissues play the by the availability of specific essential amino acid8. dominant role instead of the immune cells16. In this It is not clear how allergens break tolerance. model, an “epithelial mesenchymal trophic unit” is Specific properties of allergens may be involved in the starting point of allergic sensitization and the sensitization. Many allergens such as the dust immune cells play a passive role and become mite allergens Der p1and Der p3 contain protease activated as the result of exposure to foreign activity and their allergenicity has been shown to antigens that gain access into the subepithelial require protease activity9. Protease activity may tissues because of defects in epithelial integrity and disrupt the tight junctions in airway epithelium, function. This concept was proposed because of the compromise its barrier function and allow access of finding that many genetic polymorphisms associated allergens to the local immune system. The protease with asthma are in those genes expressed in activity may also cleave certain cell surface epithelial or mesenchymal tissues, for example, molecules resulting in abnormal cellular signaling. It ADAM3317. This is somewhat surprising since one was shown that the Der p1 may also break tolerance would expect to see the association with only by down-regulating IDO expression in a protease- polymorphisms of genes expressed in the immune dependent manner10. Some other non-protease system. A logical explanation of this finding is that 114 Airway allergy and viral infection the genetic polymorphisms alter gene expression damaging the developing airway and immune and function in epithelial cells and subepithelial system or merely unmasks the genetic predisposition mesenchymal cells causing some functional defects. to asthma, providing that there are common genetic Since the main function of the epithelium is to predispositions to viral infection and asthma21. Viral provide a barrier between the external environment infection can damage the developing airway and and body tissues, it is reasonable to hypothesize that leads to airway remodeling which causes airway epithelial defects may lead to over-exposure to narrowing leading to airflow limitation and wheeze. foreign materials such as allergens. This over- Viral infection can cause an increase of DC numbers exposure may lead to the breakdown and failure of in the lung22, which can increase the chance of the immune tolerance16. Tissue
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