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Asthma is a heterogeneous chronic inflammatory airway disease. A majority of patients with severe asthma have high levels of type 2 cytokines and cells in the blood, sputum and lung tissue. The processes of regulating these type 2 responses are not fully understood. We used an epithelial cell and PBMC co-culture experimental system to determine whether epithelial cells were able to regulate type 2 cytokine release by PBMC either directly or through a transwell. PBMC cultured with IL-2 produced 513.88 +/- 397.77 (n=5) pg IL-13 per 106 cells +/- SD, 10.22 +/- 3.43 (p=0.0036, n=3) when cultured with A549, 72.18 +/- 71.86 (p=0.036, n=3) with BEAS2B and 32.94 +/- 32.77 (p=0023, n=4) with 16HBE epithelial cell lines. Culture of A549, BEAS2B and 16HBE cells with PBMC across a transwell showed similar levels of inhibition and was epithelial cell number dependent. Culturing PBMC with healthy HBEC cells across a transwell reduced IL-13 release from 549.77 +/- 89.58 to 179.53 +/- 70.16, p<0.0001. Culture media from epithelial cells was able to inhibit IL-13 release from IL-2 stimulated PBMC in a dose dependent fashion. When supernatants were split into size fractions, A549 and HBEC supernatants less than 3KDa were more effective at inhibiting IL-13 release than those above 3KDa. The further characterisation of these mediators could elucidate important molecules in the regulation of asthma which in turn could lead to novel anti-inflammatory strategies.



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