Iordanes Karagiannides1, Charalabos Pothoulakis. 1. Gastrointestinal Neuropeptide Center, Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Abstract
PURPOSE OF REVIEW: The purpose of this review is to present recent data on how obesity-associated conditions may affect innate immunity and its role in the development of gut inflammation. RECENT FINDINGS: Here we present studies that demonstrate the participation of adipose tissue components in the generation of inflammation. More specifically, we describe increases in the release of proinflammatory cytokines during obesity as well as the expression of receptors involved in innate immune responses by adipocytes. Furthermore, we present data on the involvement of adipose tissue-specific molecules (adipokines) in the generation of an environment that is favorable for diseases with an immune cause and in some cases (leptin) directly contribute to the development of inflammatory bowel disease. Finally, we present evidence supporting a putative association between obesity and gut inflammation through the link of inflammation with angiogenesis and neovascularization and the favorable conditions created for these responses in obesity. SUMMARY: We believe that obesity-related systemic changes may create conditions that predispose to the development of gut inflammation or even worsen the progression of ongoing disease.
PURPOSE OF REVIEW: The purpose of this review is to present recent data on how obesity-associated conditions may affect innate immunity and its role in the development of gut inflammation. RECENT FINDINGS: Here we present studies that demonstrate the participation of adipose tissue components in the generation of inflammation. More specifically, we describe increases in the release of proinflammatory cytokines during obesity as well as the expression of receptors involved in innate immune responses by adipocytes. Furthermore, we present data on the involvement of adipose tissue-specific molecules (adipokines) in the generation of an environment that is favorable for diseases with an immune cause and in some cases (leptin) directly contribute to the development of inflammatory bowel disease. Finally, we present evidence supporting a putative association between obesity and gut inflammation through the link of inflammation with angiogenesis and neovascularization and the favorable conditions created for these responses in obesity. SUMMARY: We believe that obesity-related systemic changes may create conditions that predispose to the development of gut inflammation or even worsen the progression of ongoing disease.
Authors: Piero Portincasa; Leonilde Bonfrate; Mohamad Khalil; Maria De Angelis; Francesco Maria Calabrese; Mauro D'Amato; David Q-H Wang; Agostino Di Ciaula Journal: Biomedicines Date: 2021-12-31