Fig. 7: Hypoxia signature was dependent on pathogen’s invasion and colonization of the PP in the mouse typhoid disease model.

a–c Mice were orally infected with either wild-type S. Typhimurium or a triple mutant strain (invA/fliC/fljB mutant). a Bacterial burden in the PP of wild-type (n = 5) and triple mutant-infected mice (n = 4) was quantified by colony-forming units (CFU). Box plots show the median, 25^th and 75^th percentiles, with whiskers representing the range excluding outliers. P-value is calculated using a two-sided two-sample t-test (t(7) = 2.55, p = 0.038, 95% Confidence Intervals = 0.15–3.83) (b) PCA plot of the two leading principal components shows separation between PP of naïve (n = 4), wild-type infected (n = 4), and triple mutant-infected (n = 3) mice. c, d GSEA comparing wild-type infected PP at 72 hpi versus naïve PP (c), and triple mutant-infected PP versus naïve PP (d) identifies strain-specific pathways (highlighted in blue for wild-type strain and in turquoise for mutant strain). The hypoxia pathway is significantly up-regulated only in PP infected with the wild-type strain, but not in triple mutant infected PP. The x-axis shows significance as -log₁₀(q-value), adjusted for multiple comparisons using FDR.