PT - JOURNAL ARTICLE AU - Laura Cottey AU - Nivenka Jayasekera AU - Hans-Michael Hiatchi AU - Ben Green AU - Chris Grainge AU - Peter Howarth TI - Airway epithelial toll-like receptor expression in asthma and its relationship to disease severity DP - 2011 Sep 01 TA - European Respiratory Journal PG - p3842 VI - 38 IP - Suppl 55 4099 - http://erj.ersjournals.com/content/38/Suppl_55/p3842.short 4100 - http://erj.ersjournals.com/content/38/Suppl_55/p3842.full SO - Eur Respir J2011 Sep 01; 38 AB - Asthma is classically considered a Th2 mediated disease. However severe, treatment-resistant disease is more heterogeneous and often associated with airway neutrophil recruitment. This could be due to altered airway bacterial colonisation. Bacteria express molecular patterns that are recognised as non-self by pattern recognition receptors expressed on innate cell surfaces such as Toll-like receptors (TLR's). This study has investigated the expression of mRNA for TLR-2, -4 and -5 in airway epithelial cells in asthmatics and healthy volunteers.Epithelial brushings were obtained from the large airways at bronchoscopy from 18 healthy non-asthmatic volunteers and 34 asthmatic volunteers. The asthmatic group comprised 7 non-steroid treated and 27 steroid treated asthmatics. RT-qPCR analysis was performed on extracted RNA for TLR-2,-4 and -5 and IL-8.Gene expression for TLR-2 (p=0.008) and TLR-4 (p=0.012) was significantly increased within the asthmatic sample compared to healthy subjects whilst TLR5 expression did not differ significantly. IL-8 mRNA was also increased in the asthmatic population (p=0.007) compared to that of healthy subjects. These significant differences from the healthy population were also individually present in both the mild and severe asthmatics groups, with no significant difference being evident between mild and severe asthma.These findings reveal up-regulation of epithelial gene expression for TLR family members and IL-8 relevant to bacterial responses within the airways. These features are indicative of ongoing innate immune airway responses in asthma. The relevance of this to clinical disease expression requires understanding.