A combination of dietary advice and provision of commercially available food items enabled subjects with a low-moderate habitual consumption of WG to substantially increase their WG intake, but there was little effect on blood biochemical markers, body composition, BP, fecal measurements, or gut microbiology. This trial was registered at www.controlled-trials.com as ISRCTN36521837.

BackgroundThe preimplantation embryo is sensitive to culture conditions in vitro and poor maternal diet in vivo. Such environmental perturbations can have long-lasting detrimental consequences for offspring health and physiology. However, early embryo susceptibility to other aspects of maternal health and their potential long-term influence into adulthood is relatively unexplored. In this study, we established an in vivo mouse model of maternal periconceptional systemic inflammation by intraperitoneal lipopolysaccharide (LPS) administration on the day of zygote formation and investigated the consequences into adulthood.ResultsIn the short term, maternal LPS challenge induced a transient and typical maternal sickness response (elevated serum proinflammatory cytokines and hypoactive behaviour). Maternal LPS challenge altered preimplantation embryo morphogenesis and cell lineage allocation, resulting in reduced blastocyst inner cell mass (ICM) cell number and a reduced ICM:trophectoderm cell ratio. In the long term, diverse aspects of offspring physiology were affected by maternal LPS treatment. Whilst birthweight, growth and adult blood pressure were unaltered, reduced activity in an open-field behaviour test, increased fat pad:body weight ratio and increased body mass index were observed in male, but not female, offspring. Most importantly, the maternal LPS challenge caused corticosterone-independent blunting of the serum proinflammatory cytokine response to innate immune challenge in both male and female offspring. The suppressed state of innate immunity in challenged offspring was dose-dependent with respect to the maternal LPS concentration administered.ConclusionsThese results demonstrate for the first time that the preimplantation embryo in vivo is sensitive to maternal systemic inflammation, with effects on blastocyst cell lineage allocation and consequences for behaviour, adiposity and innate immune response in adult offspring. Critically, we identify a novel mechanism mediated through maternal-embryonic interactions that confers plasticity in the development of the innate immune system, which is potentially important in setting postnatal tolerance to environmental pathogens. Our study extends the concept of developmental programming of health and disease to include maternal health at the time of conception.

From implantation of the embryo through to birth, successful pregnancy relies upon the promotion of a tolerogenic uterine environment to allow the foetus to thrive. 1 Simultaneously, and of equal importance, the maternal inflammatory response must be conserved to protect the mother and foetus against pathogens. 2 This "paradox" of pregnancy, first described by Sir Peter Medawar in the 1950s, 1 has prompted investigation into the immunology of pregnancy, particularly where it may be dysfunctional. Chronic histiocytic intervillositis (CHI), also known as chronic intervillositis (CI), chronic intervillositis of unknown aetiology

Despite the dramatic increase in WG consumption, there were no effects on phenotypic or functional immune parameters, markers of inflammation or metabolic markers.