Fig 1: Neutralization of IFNγ and TNF alter the inflammatory environment induced by secondary challenge. Naïve and LCMV-immune mice were challenged with Lm-gp61 and some groups of mice were additionally treated with neutralizing antibodies to IFNγ or TNF. Bar plots show the concentration of (A) IFNγ; (B) TNF and (C) IL-6 in the serum of the indicated treatment groups at day 1 or 3 after Lm-gp61 challenge. n = 7–8 mice per group, data are representative of two separate experiments.
Fig 2: Heterologous challenge with Lm-gp61 induces increased levels of serum IFNγ. Naïve and LCMV-immune mice were challenged with Lm-gp61. Cytokine concentrations in the serum at day 1 and 3 post-infection were assessed using a cytokine bead array for (A) IFNγ; (B) IL-12p70; (C) TNF; (D) IL-1β; (E) IL-10; and (F) IL-6. n = 8 mice/group, data are pooled from two separate experiments. Dotted lines indicate limit of detection for the assay.
Fig 3: Hypothesis schema depicting the mechanism of L-fucose in HSD-promoted inflammation. Mice received CD or HSD for 8 consecutive weeks. The CD-fed mice possess a normal gut microbiota, which leads to a higher abundance of an intestinal microbial metabolite L-fucose. L-fucose has anti-inflammatory properties, and when CD-fed mice are stimulated with inflammatory injuries, the inflammatory response in CD-fed mice is controlled at a reasonable level. On the contrary, the HSD consumption altered the composition of gut microbiota in the HSD-fed mice and significantly reduced the abundance of L-fucose. When HSD-fed mice are stimulated with inflammatory injuries, reduced L-fucose levels in the gut contributed to a more substantial inflammatory response, as evidenced by the increased accumulation of inflammatory cells and elevated levels of inflammatory cytokines including TNF-α, IL-6, and MCP-1.
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