Asthma is a serious inflammatory condition of the lungs which affects 5.4 million people in the UK. Asthma patients have an altered lung microbiota (Huang and Boushey, 2014). Free fatty acid receptor 2 (FFA2) is a G protein coupled-receptor responding to short chain fatty acids, metabolites of commensal bacteria. This study aims to characterize the effect of a murine model of asthma on FFA2 expression levels in the lungs. An asthma-like condition was induced in C57/Bl6NCrl mice by inoculation with house dust mite (HDM) protein. Briefly, mice were anaesthetized with isoflurane, and a 20 µL drop of HDM or saline applied to the nose. Mice were treated in this manner for 10 days, then terminated at 1, 2, 5 and 9 days post treatment. These studies were performed at AstraZeneca, Mölndal, with local ethical approval. After termination, the lungs were lavaged with PBS and cells in the bronchoalveolar lavage fluid (BALf) counted. The colon and lungs were removed for RNA extraction, and Ffar2 expression analysis with SYBR green qPCR. Data are presented as means ±SEM. HDM inoculation triggered an inflammatory response in C57 mice, with an increase of eosinophils, neutrophils and total lymphocytes in BALf. Cell numbers were highest after 24 hours, and decreased over time (table 1). Levels of FFA2 message in the lungs followed the same pattern (table 2), while FFA2 in the colon did not change after HDM treatment. Statistical tests were 2-way ANOVA and Student’s unpaired t-test, as appropriate. This study demonstrates that FFA2 is expressed in healthy lung tissue, and that expression is dramatically increased during HDM challenge. It is likely that the FFA2 receptor is present on the white blood cells, as opposed to smooth muscle or epithelium. As a control, another tissue well known to express FFA2, the colon, did not show any increase in FFA2 expression during asthmatic symptoms. To further this study, the microbiota of both gut and colon will be sequenced, and the HDM protocol repeated in Ffar2-/- mice to see if this inhibits white blood cell infiltration.