Fig. 5: IgA-coated BEVs promote pro-inflammatory cytokine release in CD89+ cells.
From: Enrichment of human IgA-coated bacterial vesicles in ulcerative colitis as a driver of inflammation

a IL-8 response in CD89+CD14+CD11b+ U937 monocytes exposed to uncoated or IgA-coated BEVs from B. fragilis and L. acidophilus (BEVsB/L and IgA-BEVsB/L), uncoated or IgA-coated hEVs or 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 response in CD89+CD14+CD11b+ U937 monocytes exposed to uncoated or IgA-coated BEVs from B. fragilis and L. acidophilus (BEVsB/L and IgA-BEVsB/L), uncoated or IgA-coated hEVs or soluble IgA alone. Dosage of the effector samples given a total protein biomass determined Bradford is indicated. Incubation with saline served as mock-treated control (co). (n = 8 for uncoated hEVs; all other data sets n = 9). c IL-8 response in CD89-negative human intestinal organoid-derived monolayers from two healthy donors exposed to 5 µg uncoated or IgA-coated BEVs from B. fragilis and L. acidophilus (BEVsB/L and IgA-BEVsB/L). Lack of CD89 expression was confirmed by FACS (Fig. 3a). Data is presented as median ± interquartile range (n = 5 for each data set). d IL-8 (left) and IL-6 (right) response in CD14+ human monocytes isolated from three healthy donors exposed to 5 µg uncoated or IgA-coated BEVs from B. fragilis and L. acidophilus (BEVsB/L and IgA-BEVsB/L). CD89 expression was confirmed by FACS analysis (Fig. 3b). Data is presented as median ± interquartile range (n = 4 for donor 1, n = 5 for donor 2, and n = 7 for donor 3). 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 between uncoated and IgA-coated BEVs was evaluated by two-sided Mann–Whitney U-test. Source data are provided as a Source Data file.