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Fig. 3 | Microbiome

Fig. 3

From: Colonocyte-derived lactate promotes E. coli fitness in the context of inflammation-associated gut microbiota dysbiosis

Fig. 3

Lactate availability utilization by E. coli in a mouse model of non-infectious colitis. A Schematic of treatment regimens. B, C Il10-deficient mice received piroxicam-enriched feed to induce intestinal inflammation. After 7 days, mice were colonized with a 1:1 mixture of the MP1 E. coli wild-type strain (WT) and an isogenic mutant lacking the indicated lactate dehydrogenase. The abundance of the wild-type strain and the mutant in the cecal (B) and colon (C) content was determined 3 days after inoculation. The competitive index represents the ratio of WT and mutant recovered from the cecum content of mice at the end of the colitis treatment. D–G Groups of Il10-deficient mice received piroxicam-enriched feed and samples were collected at the indicated time points. D mRNA levels of Nos2 (black bars) and Tnfa (gray bars), normalized to Gapdh, in the cecal tissue as determined by RT-qPCR. E Combined histopathology scores describing the severity of inflammation in the cecal tissue. F, G Concentrations of lactate (F) and butyrate (G) in the cecum content measured by GC/MS. Columns and error bars represent the geometric mean and geometric standard deviation, respectively. In panel E, columns and error bars represent the mean and the standard deviation. Each dot reflects data from one animal. Statistical significance was determined using the Kruskal-Wallis test. *, p<0.05; **, p<0.01; ***, p<0.001

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