@article {Porsbjerg1716, author = {Celeste Porsbjerg and Katherine Baines and Asger Sverrild and Vibeke Backer and Peter Gibson}, title = {Eosinophilic airway inflammation is associated with increased TLR2 and TLR4 expression in adult asthmatics}, volume = {44}, number = {Suppl 58}, elocation-id = {1716}, year = {2014}, publisher = {European Respiratory Society}, abstract = {Background: It is increasingly recognised that innate immune pathways are involved in asthma: Toll like receptors (TLR) are up regulated in acute and fatal asthma, and in neutrophilic asthma. TLR activation may also induce a Th2 type response, but little evidence is available in humans.Aim: We hypothesized eosinophilic airway inflammation to be associated with increased TLR expression, independently of other causative factors such as neutrophilic inflammation or airflow obstruction.Methods: Asthma patients with at least one objective marker of asthma (Airway hyperresponsiveness ((AHR) to mannitol or methacholine), or reversibility to beta-2-agonist) were examined with induced sputum for differential cell count and TLR2 and TLR4 mRNA expression using real-time PCR.Results: Induced sputum was obtained in 66 asthma patients (age 32 years (13.6), 56\% females, median asthma duration: 1 year (range 0-56 years), FEV1\% of predicted: 93.2\% ({\textpm}16.2) ACQ 1.4 ({\textpm}1.0)). Airway eosinophilia (\> 3\%) was found in 29 \% (n=19) and neutrophilia (\> 61\%) in 16 \% (n=10).In a regression analysis, eosinophilic and neutrophilic inflammation, as well as post bronchodilator FEV1\%, were independently associated with the level of TLR2 expression (Eosinophils \> 3\%, Beta: 0.31, p= 0.007. Neutrophils \> 61\%: 0.31, p=0.007, FEV1\% post SABA: -0.29, p=0.011), whereas TLR4 was only associated with eosinophilia (Beta: 0.29, p=0.018). Duration of asthma, asthma control, AHR and atopy were not predictors of an increased TLR expression.Conclusion: Airway eosinophilia was associated with increased airway TLR2 and TLR4 mRNA expression, independently of neutrophilic inflammation or chronic airflow obstruction.}, issn = {0903-1936}, URL = {https://erj.ersjournals.com/content/44/Suppl_58/1716}, eprint = {https://erj.ersjournals.com/content}, journal = {European Respiratory Journal} }