Absence of a role for interleukin-13 in inflammatory bowel disease

PAOLO BIANCHERI; ANTONIO DI SABATINO; FRANCESCA AMMOSCATO; FEDERICA FACCIOTTI; FLAVIO CAPRIOLI; RENATA CURCIARELLO; SYED S. HOQUE; AMIR GHANBARI; IJEOMA JOE-NJOKU; PAOLO GIUFFRIDA; LAURA ROVEDATTI; JENS GEGINAT; GINO R. CORAZZA; THOMAS T. MACDONALD

EUROPEAN JOURNAL OF IMMUNOLOGY

WILEY-V C H VERLAG GMBH

Lugar: Weinheim; Año: 2014 vol. 44 p. 370 - 385

0014-2980

IL-13 has been implicated in the pathogenesis of ulcerative colitis (UC), and may have arole in animal models of gut fibrosis. We studied the involvement of IL-13 in inflammationand fibrosis in UC and Crohn?s disease (CD). Intestinal biopsies and anti-CD3/CD28- oranti-CD2/CD28-stimulated lamina propria mononuclear cells from UC and CD patientsand control subjects were cultured, and IL-13, IL-4, IL-5, IL-17A and IFN-γ productionwas measured. Mucosal IL-13-producing cells were characterised by flow cytometry. Gutexplants from strictured CD, non-strictured CD and healthy donors were cultured exvivo, and secreted IL-13, IL-1β and collagen were measured. IL-13 production by mucosalexplants and activated lamina propria mononuclear cells did not differ between CD, UCand control subjects, and was at least a log lower than IFN-γ and IL-17A. IL-13-producingcells, and in particular natural killer T cells, were uniformly low in all groups. IL-4 andIL-5 were undetectable in culture supernatants. Explants of CD strictures produced lowamounts of IL-13, whereas IL-1β and collagen were elevated. We could not confirm thatUC or strictured CD are associated with elevated IL-13 production. These data suggestthat an anti-IL-13 Ab would not be an appropriate therapeutic strategy in inflammatorybowel disease.