Tudy in an animal model of chronic asthma suggests that long-term allergen challenge may well be linked with a reduce in expression of kind I and kind II interferons, as well as with borderline alterations in type III interferons [59]. Intriguingly, these authors also reported decreased production of other pro-inflammatory cytokines, for instance IL-1 and IL-12, in response to RV infection. We recognise the inherent weaknesses of in vitro research. Furthermore, our experiments utilised undifferentiated immersion cultures of AEC in lieu of differentiated airliquid interface cultures. Notwithstanding these limitations, having said that, we think that our data shed new light around the complex interplay amongst respiratory viral infections, the host cytokine response, and acute inflammation in the airways in exacerbations of allergic asthma.research. RKK conceived the study, participated in its design and style and co-ordination, and drafted the manuscript. All authors study and authorized the final manuscript. Acknowledgements Work in the authors’ laboratories is supported by grants from NHMRC Australia. The funding agency had no role inside the collection, evaluation, and interpretation of information; in the writing with the manuscript; or inside the decision to submit the manuscript for publication. Author information 1 Department of Pathology, School of Medical Sciences, UNSW Australia, Sydney 2052, Australia. 2Respiratory Cellular and Molecular Biology, Woolcock Institute of Health-related Analysis, University of Sydney, Sydney 2037, Australia. three Otorhinolaryngology Hospital, The very first Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China. 4School of Healthcare Molecular Biosciences, University of Technologies Sydney, Sydney 2007, Australia. Received: 13 June 2014 Accepted: 21 AugustConclusions Collectively, our final results recommend that the Th2 cytokine atmosphere which prevails in allergic asthma could promote enhanced production of pro-inflammatory mediators by AEC in response to respiratory viral infection, but is unlikely to play a function in any impairment of antiviral host defences in asthmatics.Abbreviations AEC: Airway epithelial cells; dsRNA: Double-stranded RNA; HPRT: Hypoxanthine-guanine phosphoribosyltransferase; IFN: Interferon; IL: Interleukin; RV: Rhinovirus(es); TLR: Toll-like receptor; TSLP: Thymic stromal lymphopoietin.888725-91-5 custom synthesis Competing interests The authors declare that they have no competing interests.4-(Dimethylamino)but-2-ynoic acid site Authors’ contributions CH supervised the research on MLE-12 cells plus the molecular biological research on human AEC.PMID:24507727 Q-XZ performed the cell culture and enzyme immunoassays for human AEC. RS performed the cell culture and a lot of the molecular biological studies on MLE-12 cells. LG performed the molecular biological studies on human AEC. BO supervised a lot of the human AECReferences 1. Reddel HK, Taylor DR, Bateman ED, Boulet LP, Boushey HA, Busse WW, Casale TB, Chanez P, Enright PL, Gibson PG, de Jongste JC, Kerstjens HA, Lazarus SC, Levy ML, O’Byrne PM, Partridge MR, Pavord ID, Sears MR, Sterk PJ, Stoloff SW, Sullivan SD, Szefler SJ, Thomas MD, Wenzel SE: An official American Thoracic Society/European Respiratory Society statement: asthma handle and exacerbations: standardizing endpoints for clinical asthma trials and clinical practice. Am J Respir Crit Care Med 2009, 180:59?9. 2. Bahadori K, Doyle-Waters MM, Marra C, Lynd L, Alasaly K, Swiston J, FitzGerald JM: Financial burden of asthma: a systematic evaluation. BMC Pulm Med 2009, 9:24. 3. Jackson DJ, Johnston SL: The function of.
