RT Journal Article SR Electronic T1 The release of interleukin-26 from alveolar type II cells and its response to stimuli from Gram-negative and Gram-positive bacteria JF European Respiratory Journal JO Eur Respir J FD European Respiratory Society SP PA5453 DO 10.1183/13993003.congress-2019.PA5453 VO 54 IS suppl 63 A1 Graziella Tabacaru A1 Anders Linden A1 Karlhans Che YR 2019 UL http://erj.ersjournals.com/content/54/suppl_63/PA5453.abstract AB Background: The cellular sources of IL-26 in human airways include T-lymphocytes, bronchial epithelial cells and alveolar macrophages. Here, IL-26 is markedly increased in response to endotoxin, an archetype component of Gram-negative bacteria (GNB). However, the corresponding response to Gram-positive bacteria (GPB) in the airways is not known. Moreover, alveolar type II cells, which play a key role in innate immune responses to bacteria have not been investigated in terms of IL-26 release.Aims and Objectives: To characterize whether alveolar type II epithelial cells release IL-26 protein inherently, and in response to GNB and GPB.Methods: A model of human alveolar type II epithelial cells (A549 cells) was utilized. The TLR1/2 (Pam3CSK4) and TLR6 (Pam2CGDPKHPKSF) ligands represented a stimulus from GPB. The TLR4 ligand (LPS) represented a stimulus from GNB. Moreover, The TLR5 ligand (flagellin) represented a stimulus from both GPB and GNB. Cells were stimulated (0.1 & 1ug/mL) during 3-24 hours (h). We quantified IL-26 protein concentrations in cell-free conditioned media (ELISA).Results: There was a time-dependent increase release of inherent IL-26 protein in cell-free conditioned media. TLR1/2 stimulation (1µg/mL) increased IL-26 at the 24h time-point whereas TLR4 stimulation (1µg/mL) increased IL-26 at the 6h time-point. TLR5 (1ug/mL) and TLR6 (0. 1 & 1µg/mL) stimulation increased IL-26 at 3, 6 and 24h time points.Conclusions: A model of human alveolar type II cells releases IL-26 in response to stimuli from GNB and GPB. Further exploration of the involvement of alveolar type II cells and IL-26 in airway disease affecting host defense is warranted.FootnotesCite this article as: European Respiratory Journal 2019; 54: Suppl. 63, PA5453.This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).