De novo assembly and annotation of the whole genomic analysis of Vibrio campbellii RT-1 strain, from infected shrimp: Litopenaeus vannamei.

OBJECTIVES: This study aimed to sequence the whole genome of Vibrio campbellii RT-1 strain. METHODS: V. campbellii strain was isolated from an infected shrimp, Litopenaeus vannamei collected from aquaculture ponds, India (12.1899° N, 79.9249° E). The whole genome sequencing (WGS) was performed using the Illumina Hiseq 2500 platform and assembled de novo using SPAdes and Velvet optimiser. Furthermore, the gene prediction and annotation were performed by a rapid prokaryotic genome tool-Prokka. RESULTS: The genome of V. campbellii RT-1 strain has one circular chromosome with 6327218 bp long. V. campbellii RT-1 strain contains 5787 predicted genes with an average of 45% GC content. A total of 86 known genes associated with pathogenicity were identified and 28 genes were found to be responsible for virulence factors. Furthermore, 1112 unigenes were subjected to Gene Ontology (GO) terms, and 4895 predicted proteins were annotated with Clusters of orthologous (COGs) functional groups. CONCLUSIONS: The phylogenetic position of V. campbellii RT-1 strain was established through whole genome sequencing and genomic tools which provides a strong platform to further study on genomic alterations and phenotype of V. campbellii.

The Role of Hypothalamic NF-κB Signaling in the Response of the HPT-Axis to Acute Inflammation in Female Mice.

A large proportion of critically ill patients have alterations in the hypothalamus-pituitary-thyroid (HPT) axis, collectively known as the nonthyroidal illness syndrome. Nonthyroidal illness syndrome is characterized by low serum thyroid hormone (TH) concentrations accompanied by a suppressed central component of the HPT axis and persistent low serum TSH. In hypothalamic tanycytes, the expression of type 2 deiodinase (D2) is increased in several animal models of inflammation. Because D2 is a major source of T3 in the brain, this response is thought to suppress TRH expression in the paraventricular nucleus via increased local bioavailability of T3. The inflammatory pathway component RelA (the p65 subunit of nuclear factor-κB) can bind the Dio2 promoter and increases D2 expression after lipopolysaccharide (LPS) stimulation in vitro. We aimed to determine whether RelA signaling in tanycytes is essential for the LPS-induced D2 increase in vivo by conditional elimination of RelA in tanycytes of mice (RelA(ASTKO)). Dio2 and Trh mRNA expression were assessed by quantitative in situ hybridization 8 or 24 hours after saline or LPS injection. At the same time points, we measured pituitary Tshß mRNA expression and serum T3 and T4 concentrations. In RelA(ASTKO) mice the LPS-induced increase in Dio2 and decrease in Trh mRNA levels in the hypothalamus were reduced compared with the wild-type littermates, whereas the drop in pituitary Tshß expression and in serum TH concentrations persisted. In conclusion, RelA is essential for the LPS-induced hypothalamic D2 increase and TRH decrease. The central changes in the HPT axis are, however, not required for the down-regulation of Tshß expression and serum TH concentrations.