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.

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BackgroundGut microbial colonization and development of immune competence are intertwined and are influenced by early-life nutritional, environmental, and management factors. Perturbation of the gut microbiome at young age affects the crosstalk between intestinal bacteria and host cells of the intestinal mucosa.ResultsWe investigated the effect of a perturbation of the normal early life microbial colonization of the jejunum in 1-day old chickens. Perturbation was induced by administering 0.8 mg amoxicillin per bird per day) via the drinking water for a period of 24 h. Effects of the perturbation were measured by 16S rRNA profiling of the microbiome and whole genome gene expression analysis. In parallel to what has been observed for other animal species, we hypothesized that such an intervention may have negative impact on immune development.Trends were observed in changes of the composition and diversity of the microbiome when comparing antibiotic treated birds with their controls. in the jejunum, the expression of numerous genes changed, which potentially leads to changes in biological activities of the small intestinal mucosa. Validation of the predicted functional changes was performed by staining immune cells in the small intestinal mucosa and a reduction in the number of macrophage-like (KUL01+) cells was observed due to a direct or indirect effect of the antibiotic treatment. We provide evidence that a short, early life antibiotic treatment affects both the intestinal microbiota (temporarily) and mucosal gene expression over a period of 2 weeks.ConclusionThese results underscore the importance of early life microbial colonization of the gut in relation to immune development and the necessity to explore the capabilities of a variety of early life dietary and/or environmental factors to modulate the programming for immune competence in broilers.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-017-3625-6) contains supplementary material, which is available to authorized users.

Human familial neurohypophyseal diabetes insipidus (FNDI) is an autosomal dominant endocrine disorder that presents in early childhood as excessive drinking and urination as a consequence of a progressive loss of secretion of vasopressin (VP) from posterior pituitary nerve terminals. Mutations in the VP gene have been implicated as the cause of FNDI, but the mechanisms by which these mutants manifest their pathology, and prevent the secretion of the co‐expressed wild‐type protein, are unknown. One hypothesis suggests that mutant precursors are toxic, and stop the synthesis of wild‐type VP by killing expressing cells. Another hypothesis suggests that aberrant interactions between mutant and wild‐type precursors might directly inhibit the elaboration or secretion of the products of the normal allele. We have tested these hypotheses using new animal models‐‐transgenic rats that express an FNDI mutant VP gene that encodes a truncated precursor (Cys67stop). Cell‐specific and inducible expression of the Cys67stop mutation in rat VP hypothalamic neurons does not result in cell death or atrophy. Rather, expression of the FNDI mutant causes a neuronal pathology characterized by distorted structures in the cell body that are labeled by antisera that recognize endoplasmic reticulum (ER) markers, and that accumulate both mutant and wild‐type VP gene products. This is accompanied by an increase in the abundance of the mannose‐6‐phosphate receptor (MPR), a marker of endosome‐lysosome activity. We suggest that FNDI in humans may be initiated, as in our transgenic rat model, by the trapping of wild‐type VP gene products within an ER, which is targeted for lysosomal degradation by autophagy.

BackgroundStreptococcus suis is a zoonotic pathogen that causes infections in young piglets. S. suis is a heterogeneous species. Thirty-three different capsular serotypes have been described, that differ in virulence between as well as within serotypes.ResultsIn this study, the correlation between gene content, serotype, phenotype and virulence among 55 S. suis strains was studied using Comparative Genome Hybridization (CGH). Clustering of CGH data divided S. suis isolates into two clusters, A and B. Cluster A isolates could be discriminated from cluster B isolates based on the protein expression of extracellular factor (EF). Cluster A contained serotype 1 and 2 isolates that were correlated with virulence. Cluster B mainly contained serotype 7 and 9 isolates. Genetic similarity was observed between serotype 7 and serotype 2 isolates that do not express muramidase released protein (MRP) and EF (MRP-EF-), suggesting these isolates originated from a common founder. Profiles of 25 putative virulence-associated genes of S. suis were determined among the 55 isolates. Presence of all 25 genes was shown for cluster A isolates, whereas cluster B isolates lacked one or more putative virulence genes. Divergence of S. suis isolates was further studied based on the presence of 39 regions of difference. Conservation of genes was evaluated by the definition of a core genome that contained 78% of all ORFs in P1/7.ConclusionsIn conclusion, we show that CGH is a valuable method to study distribution of genes or gene clusters among isolates in detail, yielding information on genetic similarity, and virulence traits of S. suis isolates.

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Emerging knowledge shows the importance of early life events in programming the intestinal mucosal immune system and development of the intestinal barrier function. These processes depend heavily on close interactions between gut microbiota and host cells in the intestinal mucosa. In turn, development of the intestinal microbiota is largely dependent on available nutrients required for the specific microbial community structures to expand. It is currently not known what the specificities are of intestinal microbial community structures in relation to the programming of the intestinal mucosal immune system and development of the intestinal barrier function. The objective of the present study was to investigate the effects of a nutritional intervention on intestinal development of suckling piglets by daily oral administration of fructooligosaccharides (FOS) over a period of 12 d (days 2–14 of age). At the microbiota community level, a clear “bifidogenic” effect of the FOS administration was observed in the colon digesta at day 14. The former, however, did not translate into significant changes of local gene expression in the colonic mucosa. In the jejunum, significant changes were observed for microbiota composition at day 14, and microbiota diversity at day 25. In addition, significant differentially expressed gene sets in mucosal tissues of the jejunum were identified at both days 14 and 25 of age. At the age of 14 d, a lower activity of cell cycle–related processes and a higher activity of extracellular matrix processes were observed in the jejunal mucosa of piglets supplemented with FOS compared with control piglets. At day 25, the lower activity of immune-related processes in jejunal tissue was seen in piglets supplemented with FOS. Villi height and crypt depth in the jejunum were significantly different at day 25 between the experimental and control groups, where piglets supplemented with FOS had greater villi and deeper crypts. We conclude that oral FOS administration during the early suckling period of piglets had significant bifidogenic effects on the microbiota in the colon and on gene expression in the jejunal mucosa by thus far unknown mechanisms.

Olfactory ensheathing glia (OEG) are a specialized type of glia that support the growth of primary olfactory axons from the neuroepithelium in the nasal cavity to the brain. Transplantation of OEG in the injured spinal cord promotes sprouting of injured axons and results in reduced cavity formation, enhanced axonal and tissue sparing, remyelination, and angiogenesis. Gene expression analysis may help to identify the molecular mechanisms underlying the ability of OEG to recreate an environment that supports regeneration in the central nervous system. Here, we compared the transcriptome of cultured OEG (cOEG) with the transcriptomes of cultured Schwann cells (cSCs) and of OEG directly obtained from their natural environment (nOEG), the olfactory nerve layer of adult rats. Functional data mining by Gene Ontology (GO)-analysis revealed a number of overrepresented GO-classes associated with tissue repair. These classes include "response to wounding," "blood vessel development," "cell adhesion," and GO-classes related to the extracellular matrix and were overrepresented in the set of differentially expressed genes between both comparisons. The current screening approach combined with GO-analysis has identified distinct molecular properties of OEG that may underlie their efficacy and interaction with host tissue after implantation in the injured spinal cord. These observations can form the basis for studies on the function of novel target molecules for therapeutic intervention after neurotrauma.