Figure 1.

Ablation of nociceptive neurons increases the severity of infection and delays clearance of Citrobacter rodentium. Trpv1 message in the colon (10–12 mice/group) (A) and transient receptor potential cation channel subfamily V member 1 (TRPV1) immunoreactive neurons in the nodose ganglion (B) were assessed 20 days after administration of resiniferatoxin (RTX) or vehicle (5–6 mice/group; scale bar, 30 µm). Mice subjected to sensory nociceptive ablation were assessed for host response to C rodentium infection. The bacterial burden was assessed in the feces every 3–4 days over the course of the infection (C) and adherent to the colon at 10 days postinfection (p.i.) (15–16 animals/group, 3 independent experiments, dotted line: limit of detection) (D). TRPV1^+/+ and TRPV1^−/− were infected with C rodentium, and the bacterial burden in the feces were measured every 3–4 days (E). The effect of this infection on the colonic histopathology at 10 days p.i. (F and G) was determined by crypt length in ≥20 well oriented crypts per animal (7–9 mice/group, from 3 independent experiments). Scale bar, 50 µm. Data are presented as mean ± standard error of the mean: *, P < .05, **, P < .01, and ***, P < .0001 vs uninfected mice; #, P < .05 compared with vehicle C rodentium-infected mice; Student’s t test (A and B) and two-way analysis of variance (ANOVA) (C) and one-way ANOVA (D and G) with Tukey posttest. CFU, colony-forming units; DAPI, 4’,6-diamidino-2-phenylindole; LB, Luria-Bertani.