{'fraction_non_alphanumeric': 0.018418201516793065, 'fraction_numerical': 0.0, 'mean_word_length': 5.507042253521127, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Adipokine signaling in inflammatory bowel disease.

While the incidence of inflammatory bowel disease (IBD) is still increasing, the etiology has not finally been dissected. The main hypothesis suggests that the mucosal immune system is hyperresponsive to dietary factors and commensal bacteria in genetically predisposed individuals. Burrill Crohn himself described a local hypertrophy of the mesenteric fat tissue adjacent to the segments of inflamed intestine. In addition, more recent data indicate altered local expression and serum levels of some adipocyte-derived mediators (adipokines) with immune-modulating capacities in IBD. This review focuses on the role of adipose tissue and adipokines in the immune system, with particular focus on the mucosal immune system. The available data will serve to establish a working hypothesis on how the mesenteric fat tissue contributes to the pathogenesis of Crohn's disease.