Formyl Peptide Receptors and Annexin A1: Complementary Mechanisms to Infliximab in Murine Experimental Colitis and Crohn’s Disease

• Autor(a) principal: de Paula-Silva, Marina
• Data de Publicação: 2021
• Outros Autores: da Rocha, Gustavo Henrique Oliveira, Broering, Milena Fronza, Queiroz, Maria Luíza, Sandri, Silvana, Loiola, Rodrigo Azevedo, Oliani, Sonia Maria [UNESP], Vieira, Andrea, Perretti, Mauro, Farsky, Sandra Helena Poliselli
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UNESP
• Texto Completo: http://dx.doi.org/10.3389/fimmu.2021.714138; http://hdl.handle.net/11449/229642
• topic: annexin A1; biomarkers; Crohn’s disease; dextran sodium sulfate; formyl peptide receptor; infliximab

Non-responsiveness to anti-TNF-α therapies presents relevant rates in inflammatory bowel disease patients, presenting the need to find biomarkers involved in therapeutic efficacy. Herein, we demonstrate that higher levels of colonic formyl peptide receptor 1 and annexin A1 correlate with histological recovery in Crohn’s disease patients under remission. Using the dextran sulfate sodium colitis model in mice, we suggest that infliximab induces annexin A1 expression and secretion in activated intestinal leukocytes. Conversely, this mechanism might stimulate epithelial formyl peptide receptors, inducing wound healing and consequent histological remission. Our data indicate that assessing intestinal expressions of formyl peptide receptors and annexin A1 might provide precious information on the disease activity and responsiveness to infliximab in inflammatory bowel disease patients.