Figure 8. Working model of the immunologic mechanisms underlying the amelioration of colitis in the setting of Trichuris sp. treatment.

(A) Colitis is driven by a T_H1-type inflammatory response to increased bacterial attachment and dysbiosis at the mucosal epithelium as a result of compromised barrier function. (B) Trichuris sp. elicits a mucosal T_H2-type response (including the canonical cytokines IL-4 and IL-13) that promotes mucosal wound healing and mucus production. These functions reduce bacterial attachment and restore microbial homeostasis, removing the inflammatory stimulus.