Intraperitoneal administration of the anti-IL-23 antibody prevents the establishment of intestinal nematodes in mice Gómez Samblás, María Mercedes Bernal, D. Bolado-Ortiz, A. Vilchez, S. Bolás-Fernández Espino, A. M. Trelis, María Osuna Carrillo De Albornoz, Antonio Previous studies have established that an increased Th-9 response creates a hostile environment for nematode parasites. Given that IL-23, a cytokine required for maintenance of the IL-17–secreting phenotype, has inhibitory effects on IL-9 production, we hypothesized that reducing circulating IL-23 by treatment with anti-IL-23 antibodies would reduce the establishment and development of parasitic intestinal nematodes. In this study, we show that animals treated with anti-IL-23 monoclonal antibodies showed a drastic reduction in the number of mouse pinworms (Aspiculuris tetraptera) recovered from the intestine (p < 0.001) at 23 days post-infection compared to the untreated animals. The cytokine levels in Peyer’s patches (PP) in treated and infected animals increase the expression of interleukins such as IL-25, IL-21, and IL-9, augmenting mucus production in the crypts, and boosting chemokines, such as OX40 and CCL20 in the mucosa. Our results suggest that the Th17/Th2 regulatory mechanism provoked by the administration of the anti-IL-23 antibody prevents the implantation of the intestinal nematode in mice. The diminished inflammatory IL-17 levels alter the Th9 environment perhaps as a consequence of IL-17 inhibiting IL-9 expression. These Th9 conditions may explain the successful treatment against Inflammatory Bowel Disease (IBD) both with antibodies against IL-23 or through parasitization with nematodes. 2019-02-20T12:19:19Z 2019-02-20T12:19:19Z 2018 journal article Gomez-Samblas, M. et. al. Intraperitoneal administration of the anti-IL-23 antibody prevents the establishment of intestinal nematodes in mice. Scientific Reports (2018) 8:7787 http://hdl.handle.net/10481/54806 10.1038/s41598-018-26194-x eng http://creativecommons.org/licenses/by/3.0/es/ open access Atribución 3.0 España Springer Nature