Biological therapies, such as monoclonal antibodies and infliximab (IFX), are very effective in inducing remission for moderate-to-severe IBDs ( 2, 3). Inflammatory bowel diseases (IBDs), mainly Crohn’s disease (CD) and ulcerative colitis (UC), are characterized by severe gastrointestinal inflammation ( 1). 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. Conversely, this mechanism might stimulate epithelial formyl peptide receptors, inducing wound healing and consequent histological remission. Using the dextran sulfate sodium colitis model in mice, we suggest that infliximab induces annexin A1 expression and secretion in activated intestinal leukocytes. 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. 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. 4Department of Biology, São Paulo State University (UNESP), São José do Rio Preto, São Paulo, Brazil.3Gastroenterology Service, Irmandade da Santa Casa de Misericórdia de São Paulo, São Paulo, Brazil.2Centre for Biochemical Pharmacology, The William Harvey Research Institute, Barts and The London School of Medicine, Queen Mary University of London (QMUL), London, United Kingdom.
Marina de Paula-Silva 1,2, Gustavo Henrique Oliveira da Rocha 1, Milena Fronza Broering 1, Maria Luíza Queiroz 3, Silvana Sandri 1, Rodrigo Azevedo Loiola 1, Sonia Maria Oliani 4, Andrea Vieira 3, Mauro Perretti 2 and Sandra Helena Poliselli Farsky 1*
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