Fig. 6: IgA-coated BEVs and EV fractions from UC patients promote a CD89-dependent pro-inflammatory cytokine release in mouse bone marrow derived cells (BMDC).

a IL-6 and TNF-α response in bone marrow derived cells (BMDC) from CD89^wt/wt (littermates, LM) and CD89^tg/wt (CD89-transgenic, CD89) mice exposed to uncoated or IgA-coated BEVs from B. fragilis and L. acidophilus (BEVs^B/L and IgA-BEVs^B/L) as well as soluble IgA alone. Dosage of the effector samples given by total protein biomass determined by Bradford is indicated. Incubation with saline served as mock-treated control (co). (n = 10 for each data set). b IL-6 and TNF-α response in bone marrow derived cells (BMDC) from CD89^tg/wt (CD89-transgenic, CD89) mice exposed to 1 µg IgA-coated BEVs from B. fragilis and L. acidophilus (IgA-BEVs^B/L) in the absence (-) or presence (+) of the Syk inhibitor R406. (n = 6 for each data set). c IL-6 (left) and TNF-α (right) response in bone marrow derived cells (BMDC) from CD89^wt/wt (littermates, LM) and CD89^tg/wt (CD89-transgenic, CD89) mice exposed to EV fractions derived from the non-IBD (blue) and active UC (red) group (seven randomly chosen representatives). (n = 7 for each data set). d IL-6 and TNF-α response in bone marrow derived cells (BMDC) from CD89^tg/wt (CD89-transgenic, CD89) mice exposed to 1 µg EV fractions derived from three representative active UC patients (UC1, UC2, or UC3) in the absence (-) or presence (+) of the Syk inhibitor R406. (n = 4 for each data set). a–d Data is presented as median ± interquartile range. Samples with no detectable signal were set to the limit of detection, which is indicated by a dotted line. Statistical difference in panel a was evaluated by Kruskal–Wallis (comparison of groups receiving the same BEVs^B/L dosage) with Dunn’s test. Statistical differences in all other panels [comparison of (B)EV samples with and without inhibitor or non-IBD and active UC groups] were evaluated by two-sided Mann–Whitney U-test. Source data are provided as a Source Data file.