Epithelial barrier integrity and function in paediatric asthma

[Truncated] The airway epithelium is the primary contact point with the inhaled air and provides a physical barrier defence against injurious stimuli. This barrier is achieved and maintained through a myriad of junctional complexes, however, of key interest, are the tight junctional complex proteins. Tight junctions (TJ) are located at the terminal end of the epithelial cell layer and serve to maintain structural integrity as well as regulate transepithelial permeability. Although studies have demonstrated TJ abnormalities in adults with asthma, few studies have addressed whether these abnormalities are intrinsic to asthma, are consequences of chronic inflammation, or due to atopy rather than asthma. In addition, it is unknown whether these abnormalities can be detected early in the disease progression and are correlated with disease severity.
Evidence has also demonstrated a close association between respiratory viral infections, in particular, human rhinoviruses (HRVs) and resulting asthma exacerbations. Although it has been previously shown that there is disassembly of specific TJ proteins, in particular, zonula occludens-1 (ZO-1) following HRV infection, there still remains a paucity of data on the susceptibility of the asthmatic epithelium to TJ disassembly following HRV infection, especially within a paediatric population. This presents significant rationale for the re-evaluation of the concept of epithelial barrier dysfunction in asthma as well as the effects of HRV infection on barrier integrity. Therefore, this study was conducted to study epithelial barrier function in non-asthmatic and asthmatic individuals to test the following hypotheses. Firstly, the epithelial barrier function is defective in children with asthma. Secondly, a defective barrier function in asthma is independent of atopy. Thirdly, epithelial integrity and barrier function is further compromised by HRVs in asthmatic airways compared to non-asthmatics.