BackgroundHost genetic makeup plays a role in early gut microbial colonization and immune programming. Interactions between gut microbiota and host cells of the mucosal layer are of paramount importance for a proper development of host defence mechanisms. For different livestock species, it has already been shown that particular genotypes have increased susceptibilities towards disease causing pathogens.The objective of this study was to investigate the impact of genotypic variation on both early microbial colonization of the gut and functional development of intestinal tissue. From two genetically diverse chicken lines intestinal content samples were taken for microbiota analyses and intestinal tissue samples were extracted for gene expression analyses, both at three subsequent time-points (days 0, 4, and 16).ResultsThe microbiota composition was significantly different between lines on each time point. In contrast, no significant differences were observed regarding changes in the microbiota diversity between the two lines throughout this study. We also observed trends in the microbiota data at genus level when comparing lines X and Y. We observed that approximately 2000 genes showed different temporal gene expression patterns when comparing line X to line Y. Immunological related differences seem to be only present at day 0, because at day 4 and 16 similar gene expression is observed for these two lines. However, for genes involved in cell cycle related processes the data show higher expression over the whole course of time in line Y in comparison to line X.ConclusionsThese data suggest the genetic background influences colonization of gut microbiota after hatch in combination with the functional development of intestinal mucosal tissue, including the programming of the immune system. The results indicate that genetically different chicken lines have different coping mechanisms in early life to cope with the outside world.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-015-1646-6) contains supplementary material, which is available to authorized users.
The general pattern of energy balance in early lactation was modeled. For this purpose, several lactation curves were investigated. The best fitting curve was fit in a random regression model that provided predicted energy balance curves for all lactations. By use of these curves, total energy deficit per lactation, postpartum interval of return to positive energy balance, and nadir of energy balance was determined. In predicted energy balances, nadir of energy balance was present, but variation in postpartum interval to nadir was small. First lactation cows had a smaller energy deficit in early lactation than did older cows. Differences among cows in nadir and total energy deficits in early lactation were large. Both were related to the postpartum interval to first detected estrus with a larger energy deficit and a smaller nadir corresponding to a larger postpartum interval to first detected estrus. From this study, it can be concluded that large energy deficits in early lactation delay first detected estrus.
Cystic ovarian disease (COD) is one of the most frequently diagnosed gynecological findings in dairy cattle. It causes temporary infertility and is likely to affect reproduction as well as production parameters in cows. The objectives of this study were to investigate the heritability of COD in a Dutch Black and White population and to estimate the genetic and phenotypic relationships with milk production traits. In the data set used, the overall incidence of COD was 7.7% (1204 COD diagnoses in 15,562 lactations). The farm incidence varied between 1.9 and 11.3%. The estimated heritabilities on the underlying and observable scales were 0.102 and 0.087, respectively. The genetic correlations between COD and 305-d milk, fat, and protein yields were 0.345, 0.379, and 0.441, respectively. We concluded that a genetic predisposition for COD exists in Dutch Black and White dairy cattle. The genetic correlations between COD and yield traits indicate that ongoing selection for production will increase the incidence of COD.
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