Extended Data Fig. 10: APOL9a/b control mucosal infection in a microbiota context-dependent manner.
From: Targeting symbionts by apolipoprotein L proteins modulates gut immunity
a and b, The representative flow cytometry plots (a) and binding efficiencies (b) of rmAPOL9a (5 μg/mL) or rmAPOL9b (5 μg/mL) bound with STm. Transferrin binding as a positive control (n = 3). c, Propidium iodide (PI) staining of STm after incubation with BSA (5 μg/mL), rmAPOL9a (5 μg/mL), or rmAPOL9b (5 μg/mL) for 3 h. EDTA (20 μM) plus Polymyxin B (25 μg/mL) treatment as a positive control (n = 3). d, The dynamics of CFU within the Apol9a/b+/+ or Apol9a/b–/– ileal ECs after STm in vitro infection (n = 3). e, STm quantification in the ileal lumen of Apol9a/b+/+ or Apol9a/b–/– mice after STm infection in the early or late time point (n = 6). f-h, FMT of ABX-treated Apol9a/b+/+ or Apol9a/b–/– mice with ileal microbiota from a WT C57BL/6 strain largely devoid of gut Bacteroidales, followed by STm infection. Survival curve (f, n = 8), ileal histology (day 5) (g), or bacteria quantitation (day 5) in the spleen and liver (h, n = 6) are shown. Scale bar, 10 μm. i and j, Apol9a/b+/+ or Apol9a/b–/– mice were infected intraperitoneally with STm. Survival curve (i, Apol9a/b+/+: n = 9; Apol9a/b–/–: n = 8) or bacteria quantitation (day 5) in the spleen and liver (j, n = 6) are shown. Data are representative of two independent experiments (a-j). n represents biologically independent samples (b-d) or biologically independent animals (e-j). Data are presented as mean ± SEM. Statistical analysis was performed using one-way ANOVA followed by Bonferroni post hoc test (b,c), two-tailed Student’s t-test (d,e,g,h,j), or log-rank (Mantel-Cox) test (f,i).
