RT info:eu-repo/semantics/article
T1 Human colon-derived soluble factors modulate gut microbiota composition
A1 Hevia, Arancha
A1 Bernardo Ordiz, David
A1 Montalvillo Álvarez, Enrique
A1 Al-Hassi, Hafid O.
A1 Fernández Salazar, Luis Ignacio
A1 Garrote Adrados, José Antonio
A1 Milani, Christian
A1 Ventura, Marco
A1 Arranz Sanz, Eduardo
A1 Knight, Stella C.
A1 Margolles, Abelardo
A1 Sánchez, Borja
K1 Sistema inmunológico
K1 Colon
K1 3205 Medicina Interna
AB The immune system of the gastrointestinal tract (GIT) is exposed to a large amount of foreign but harmless antigens typically derived from nutrients and commensal bacteria but sometimes deleterious when derived from infectious bacteria or viruses. Nevertheless, the GIT immune system is effective in discriminating between maintaining immune tolerance against diet and/or commensal derived antigens, and initiating immune responses against harmful invading pathogens (1). IL-15 is one of the cytokine of the innate immune response, regulating both T and natural killer (NK) cell activation and proliferation (2). The commensal microbiota plays a central role in modulating the outcome of immune responses in the GIT keeping immune homeostasis in health (3). Indeed, germ-free animals have an immature immune system and can develop inflammation, which is reversed once the microbiota is conventionalized (4). The commensal microbiota modulates several aspects of the host including the physiology and/or its nutritional status. The microbiota is also related to several diseases affecting the gut, like in inflammatory bowel diseases (IBD), and also influences diseases in distant organs (5–8). On turn, chronic gut inflammation such as happens in IBD is a risk factor for colorectal cancer. This is apparently a consequence of a high and persistent inflammation at the mucosa levels (9).
PB Frontiers Media
SN 2234-943X
YR 2015
FD 2015
LK http://uvadoc.uva.es/handle/10324/41878
UL http://uvadoc.uva.es/handle/10324/41878
LA eng
NO Frontiers in Oncology, 2015, vol. 5, 86
NO Producción Científica
DS UVaDOC
RD 24-nov-2024