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. Author manuscript; available in PMC: 2022 Jan 29.
Published in final edited form as: Cell Rep. 2022 Jan 4;38(1):110180. doi: 10.1016/j.celrep.2021.110180

Figure 3. Propionate utilization confers an advantage to S. Tm in an inflammation-dependent mechanism.

Figure 3.

(A) Streptomycin-pretreated C57BL/6 mice were inoculated with an equal mixture of WT S. Tm and ΔprpC. The competitive index in the colon content and homogenized samples from the liver or spleen was determined 4 days after infection.

(B) Streptomycin-pretreated C57BL/6 mice were inoculated with an equal mixture of the indicated S. Tm strains. The competitive index in the colonic content was determined 4 days after infection.

(C) Combined histopathology score of pathological lesions in the cecum of mice from (B) (n = 5).

(D) Representative images of hematoxylin and eosin-stained cecal tissue of mice from (C). Scale bars, 200 μm.

(E) Propionate concentration in the cecal content was determined by liquid chromatography/mass spectrometry (LC/MS) 2 days after infection.

(F) Streptomycin-pretreated C57BL/6 mice were inoculated with an equal mixture of WT S. Tm and ΔprpC. Mice received propionate supplementation (20 mM) in the drinking water for the duration of the experiment. The competitive index in the colonic content was determined 4 days after infection. Each dot represents data from one animal (biological replicate). Bars represent mean ± SEM. *p < 0.05, ***p < 0.001, ****p < 0.0001. See also Figure S3.