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. 2023 Mar 16;10:1070734. doi: 10.3389/fmed.2023.1070734

Figure 6.

Figure 6

Fuc-TLR4 signaling is indispensable for intestinal homeostasis and recovery from injury provided by gut microbes. Conventionally colonized mice recover from the chemically induced mucosal injury caused by ingestion of DSS (A). In contrast, only a fraction of mice whose microbiota are depleted by a cocktail of antibiotics recover from DSS-induced injury (BD mice). BD mice recolonized by mouse microbiota recover from this mucosal injury. Almost all TLR4−/− mutants are unable to recover from DSS mucosal injury, consistent with the essential nature of TLR4 mediating bacterial signaling needed for recovery and maintenance of mucosal integrity. BD mice that are treated with a fuc-TLR4 ligand, either UEA1 or LPS, also recover fully (B). Thus, activation of fuc-TLR4 in the absence of recolonization also allows full recovery. Thus, fuc-TLR4 signaling is necessary and sufficient for recovery of intestinal homeostasis following DSS induced injury of the gut. Conversely, neither UEA1 nor LPS can rescue TLR4−/− mice (nor MyD88−/− mice, not shown) from the injury caused by DSS treatment (C). The data are consistent with fuc-TLR4 signaling being the essential signaling agent for microbiota mediated mucosal restoration of homeostasis. (n = 15–20; *p < 0.01; **p < 0.001).