Fig. 7

Immunoglobulin A (IgA) deficiency promotes host bacteria pathogenicity during diet-induced obesity (DIO). a Body weight, b fasting glucose, c glucose tolerance (also represented by area under the curve (AUC)), and d insulin tolerance (also represented by AUC) of antibiotic-treated HFD-fed wild-type (WT) mice transplanted with fecal matter from HFD-fed IgA^−/− and IgA^wt mice (n = 5/group). e–g 16S rRNA sequencing of gut microbial populations within the distal small intestine, colon (without cecum), and cecum alone of IgA^−/− and WT mice after 14 weeks of HFD feeding and within colons of intestinal B cell adoptive transfer HFD-fed muMT⁻ (B^null) mice 2 weeks post transfer. e Relative abundances of bacterial communities at the phylum (left) and class (right) levels in the colon of HFD-fed IgA^−/− (knockout (KO)) and WT mice (n = 3/group). f Significant bacterial taxa of the colonic stool in IgA^−/− compared to WT HFD-fed mice (n = 3/group; multiple statistical testing corrected with false discovery rate (FDR) Benjamini and Hochberg approach). g Significant bacterial taxa with colonic stool of HFD-fed B cell-deficient muMT⁻ mice adoptively transferred with either IgA^−/− or WT intestinal pan B cells (n = 3/group; multiple statistical testing performed with FDR Benjamini and Hochberg approach). h Percentage of total (n = 4/group) and i high-affinity IgA-bound bacteria within the colonic contents of HFD-fed mice compared to NCD controls (n = 8/group, 2 experiments). j Frequency (left) and absolute numbers (right) of T follicular regulatory (Tfr) and T follicular helper (Tfh) CD3⁺ T cells in the colon draining  mesenteric lymph nodes (n = 5 WT, 4 IgA^−/−). Data are means ± SEM. *p < 0.05 and ** denotes p < 0.01