Surveys were conducted with cage and alternative layer production systems to assess the prevalence of fatty liver haemorrhagic syndrome (FLHS). Commercial caged laying hens of different ages from three farms in Queensland were monitored for 3 months. The mortality rate of flocks ranged from 0.8% (the youngest flock) to 11.6% (the oldest flock). Six hundred and fifty-one birds were necropsied, and approximately 40% of hens died due to FLHS. Hens kept in cages in a controlled environment shed, were at a similar risk of developing FLHS as hens kept in naturally controlled sheds, however the heavier birds in a flock were more likely to have the condition than lighter birds. In another study, layer flocks kept in cage, barn and free-range housing systems at the University of Queensland facility, were monitored for 50 weeks. Data from necropsies and performance records showed no significant differences in mortality rates between the housing systems (6.1%, 6.4% and 5.8%, for cages, barns and free-range, respectively), but the cause of mortality was different. In cages, 74% of necropsied hens died due to FLHS. In the other systems, only 0% to 5% of dead hens were diagnosed with the condition. These results are in agreement with previous Australian and overseas findings which have shown that FLHS is one of the main causes of hen death in caged flocks. Factors associated with husbandry practices in different production systems such as, restricted movement, increased production and temperature variations, influence hepatic lipid metabolism and predispose hens to FLHS.
While intron retention (IR) is now widely accepted as an important mechanism of mammalian gene expression control, it remains the least studied form of alternative splicing. To delineate conserved features of IR, we performed an exhaustive phylogenetic analysis in a highly purified and functionally defined cell type comprising neutrophilic granulocytes from five vertebrate species spanning 430 million years of evolution. Our RNA-sequencing-based analysis suggests that IR increases gene regulatory complexity, which is indicated by a strong anti-correlation between the number of genes affected by IR and the number of protein-coding genes in the genome of individual species. Our results confirm that IR affects many orthologous or functionally related genes in granulocytes. Further analysis uncovers new and unanticipated conserved characteristics of intron-retaining transcripts. We find that intron-retaining genes are transcriptionally co-regulated from bidirectional promoters. Intron-retaining genes have significantly longer 3′ UTR sequences, with a corresponding increase in microRNA binding sites, some of which include highly conserved sequence motifs. This suggests that intron-retaining genes are highly regulated post-transcriptionally. Our study provides unique insights concerning the role of IR as a robust and evolutionarily conserved mechanism of gene expression regulation. Our findings enhance our understanding of gene regulatory complexity by adding another contributor to evolutionary adaptation.
In this study, we identify molecular mediators that participate in the regulation of the immune response during corticosterone-induced stress in chickens. At 7 weeks of age, 120 chickens were exposed for 1 week to corticosterone treatment. Cytokine and chemokine mRNA expression levels were evaluated in peripheral blood and splenic lymphocytes. Expression levels of interleukin (IL)-1β, IL-6, IL-18 and transforming growth factor (TGF)-β4 mRNA were significantly up-regulated in lymphocytes 3 h after first treatment with corticosterone. TGF-β4 and IL-18 remained elevated 1 week post-initial treatment. Compared with controls, corticosterone-treated birds showed greater expression levels of chemokine (CC) mRNA, particularly for CCLi2, CCL5 (RANTES), CCL16 and CXCLi1, in peripheral and splenic lymphocytes 3 h post-initial exposure. CCLi2 mRNA was highly expressed in splenocytes at all time-points. Administration of corticosterone significantly increased circulating corticosterone concentrations and decreased total lymphocyte counts at 3, 24 h and 1 week post-initiation of corticosterone treatment. There was a positive correlation between plasma corticosterone concentrations and CCL5 and CCL16 mRNA at 3 h post-initial administration. At 1 week post-initial treatment, corticosterone concentrations correlated positively with CCL5 and negatively with IL-18 mRNA level. Conditions associated with significant changes in corticosterone levels might therefore affect the immune response by increasing pro-inflammatory responses, leading to potential modulation of the Th1/Th2 balance.