Fig. 6 | Nature Communications

Fig. 6

From: Gut-associated IgA+ immune cells regulate obesity-related insulin resistance

Fig. 6

Altered glucose metabolism in high fat diet (HFD)-fed immunoglobulin A (IgA)-deficient mice is linked to host–microbe interactions. a Intestinal permeability assay measuring concentration of fluorescein isothiocyanate (FITC)-labelled-dextran by fluorescence (left) and represented by area under the curve (AUC) (right) in collected plasma 1 and 4 h post gavage in HFD-fed wild-type (WT) and IgA−/− mice (n = 6 WT, 5 IgA−/− mice). b Serum endotoxin levels in WT and IgA−/− mice fed HFD for 14 weeks (n = 8 WT, 9 IgA−/− mice). c Distance of bacteria from intestinal epithelial cells (IECs) in HFD-fed WT and IgA−/− mice (n = 4/group). d Representative images of fluorescence in situ hybridization (FISH) and immunofluorescence staining of the bacteria (red), mucous layer (green), and intestinal cells (4′,6-diamidino-2-phenylindole (DAPI)-blue) of colon (scale bar = 50 µm; white arrows indicate representative encroaching bacteria to intestinal epithelium). e Weights (left), fasting glucose levels (left middle), blood glucose concentrations with AUCs during glucose tolerance (GTT) (right middle) and insulin tolerance test (ITT) (right) in HFD-fed IgA−/− mice treated with antibiotics in drinking water for 4 weeks compared to HFD-fed IgA−/− untreated controls (n = 5 mice/group). Frequency (left) and absolute number (right) of f CD3+ T cells, g T cell subsets, and h Foxp3+ CD4+ Tregs within the colonic lamina propria (LP) in IgA−/− mice treated with antibiotics in drinking water for 4 weeks compared to IgA−/− untreated controls fed HFD for total of 14 weeks (n = 9 WT, 10 IgA−/− mice, 2 experiments). Data are means ± SEM. * denotes p < 0.05, ** denotes p < 0.01, and *** denotes p < 0.001

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