Skip to main content
. Author manuscript; available in PMC: 2012 Jan 12.
Published in final edited form as: Nature. 2009 Oct 29;461(7268):1282–1286. doi: 10.1038/nature08530

Figure 3. Inflammatory arthritis and allergic airway disease and GPR43 deficiency.

Figure 3

a, Inflammatory arthritis (K/BxN serum injection on day 0 and 2) in Gpr43−/− mice (n = 5) versus wild-type littermates (n ≥ 3). Scores shown are mean ± s.e.m. for each time point, representative of three independent experiments. Wild-type mice are represented with closed squares, Gpr43−/− mice with open squares, controls with dashed lines, and arthritic mice with solid lines. Change in ankle thickness (top) and measurement of MPO in the peripheral blood (bottom) showed that both naive and arthritic Gpr43−/− mice had higher MPO production when stimulated with phorbol 12-myristate 13-acetate (PMA; bottom), indicating greater neutrophil activation (P < 0.001 Gpr43−/− control compared to wild-type control, P = 0.0019 Gpr43−/− compared to wild-type arthritic). Histological assessment at day 18 (right) (scale bars, 50 μm). b, OVA-induced allergic airway inflammation. BAL fluid cell counts (left), eosinophil peroxidase (EPO) activity in lung tissue (middle), and inflammation as scored by histology (right). The bottom panel shows representative haematoxylin-and-eosin-stained lung sections from wild-type and Gpr43−/− mice, and control (no OVA) mice. Scale bar, 50 μm.