Fecal microbial transplant of postinflammatory DSS stool transfers the phenotype of visceral but not somatic pain and is associated with increased stool short-chain fatty acids. (A) Experimental protocol. Antibiotic-treated recipient animals received stool via gavage from postinflammatory DSS mice, controls (CT), or vehicle (sterile phosphate-buffered saline + glycerol) alone. (B) Visceral pain was increased in mice given postinflammatory DSS stool when compared with control and vehicle. Vehicle: n = 10, CT: n = 7, DSS: n = 11, 2 experiments. One-way analysis of variance of area under the curve: ∗∗P < .01; ∗∗∗P < .001. Mice given vehicle displayed hyperalgesia at 60 mm Hg compared with mice given control stool (two-way analysis of variance, ⍵P < .05). Somatic pain, assessed by using automated Von Frey (C) and hot plate tests (D), was unaffected after fecal microbial transplant. Vehicle: n = 9, CT: n = 7, DSS: n = 8, 2 experiments. (E) Fecal butyrate and propionate are increased in the stool of recipient mice given stool from postinflammatory DSS animals when compared with those that received stool from controls or vehicle. Vehicle: n = 12, CT: n = 7, DSS: n = 11. ∗∗P < .01; ∗∗∗P < .001; ∗∗∗∗P < .0001. DSS, dextran sulfate sodium.