Extended Data Figure 4 |. CBBP mediates VRE colonization resistance by producing an inhibitor.
a, antibiotic-treated mice (n = 8 mice/2 independent experiments) received treatment by oral gavage containing CBBP, CBBPcontrol, PBS, or VRE. One week later, VRE was inoculated into the cecal content and growth was monitored 6 hours post-inoculation. b-i, antibiotic-treated mice received an oral gavage containing CBBP (n = 4 mice/1 independent experiment) or PBS (n = 3 mice/1 independent experiment). WT mice (n = 4 mice/1 independent experiment) were untreated and received no antibiotics. Four days later, RNA and proteins were extracted from the distal ileum, and RegIIIγ was measured by RT-qPCR (b) and western blot (c). Other genes involved in host- derived antimicrobial peptide production, including angiogenin-4 (Ang4) (d), defensin-1 (Def1) (e), amphiregulin (Areg) (f), and deleted in malignant brain tumors 1 (Dmbt1) (g); or inflammatory mediators including cytochrome b beta (cybb) (h) and calgranulin A (S100A8) (i) were measured by RT-qPCR. j, Rag2−/− γc−/− mice were treated with antibiotics, and orally gavaged with VRE. Three days later, VRE-dominated mice received CBBP or CBBPcontrol by oral gavage and VRE colonization was monitored by quantifying VRE in fecal samples. VRE (ATCC 700221) was used in experiments (a, j). All statistical analyses were performed using the Mann-Whitney rank sum test (two-tailed) comparing two experimental conditions. * p- value < 0.05 (= 0.0286), *** p-value < 0.001, ****p-value < 0.0001. Center values (median), error bars (range) (a); center values (mean), error bars (s.d.) (b, d-i); center values (geometric mean), error bars (geometric s.d.) (i).