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de Vos, W.

Publications and source records attributed to de Vos, W..

2 recordsLinked to original sources

Associations between infant gut microbiota and the living environment

The human gut microbiota is central to health and development of the host, and early life microbiota is affected by a range of factors that can alter the infants development for years to come. The role of the external, natural environment in shaping the gut microbiota is still largely unknown. We examined how the environment surrounding the home, in terms of land use, air quality, biodiversity, and traffic and road characteristics associate with the infant gut microbiota in the first two years of life with data from 893 children from the longitudinal birth cohort HELMi. We show that the environment has a minimal overall association with the microbiota development. Air quality explained the largest degree of variation in microbiota composition, while proximity to agriculture appeared to have a similar effect as poor air quality during the first 6 months, while open grey space and agriculture had similar associations after 6 months. The results suggest that the infant gut microbiota is not strongly dependent on the external natural environment, and that the impact of the environment is mostly mediated by exposure to pollution that may affect the hosts immune system and indirectly the gut microbiota.

microbiology↗

Gut-derived bacterial flagellin induces beta-cell inflammation and dysfunction

ObjectiveHyperglycemia and type 2 diabetes (T2D) are caused by failure of pancreatic beta cells. The role of the gut microbiota in T2D has been studied but causal links remain enigmatic. DesignObese individuals with or without T2D were included from two independent Dutch cohorts. Human data was translated in vitro and in vivo by using pancreatic islets from C57BL6/J mice and by injecting flagellin into obese mice. ResultsFlagellin is part of the bacterial locomotor appendage flagellum, present on gut bacteria including Enterobacteriaceae, which we show to be more abundant in the gut of individuals with T2D. Subsequently, flagellin induces a pro-inflammatory response in pancreatic islets mediated by the Toll-like receptor (TLR)-5 expressed on resident islet macrophages. This inflammatory response associated with beta-cell dysfunction, characterized by reduced insulin gene expression, impaired proinsulin processing and stress-induced insulin hypersecretion in vitro and in vivo in mice. ConclusionWe postulate that increased systemically disseminated flagellin in T2D is a contributing factor to beta cell failure in time and represents a novel therapeutic target. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=136 SRC="FIGDIR/small/463317v1_ufig1.gif" ALT="Figure 1"> View larger version (38K): org.highwire.dtl.DTLVardef@b719aeorg.highwire.dtl.DTLVardef@f72958org.highwire.dtl.DTLVardef@bb7af5org.highwire.dtl.DTLVardef@859c70_HPS_FORMAT_FIGEXP M_FIG C_FIG

molecular biology↗