Rabbit Anti-Human GH monoclonal antibody, clone KN219-10

Background Co-administration of human ghrelin and growth hormone (GH) reverse immunosuppression in septic aged animals, but the mechanism remains elusive. Here, we hypothesize that ghrelin and GH co-treatment restores the immune response in aged septic rats by inhibiting the production of transforming growth factor-beta (TGF-beta), an immunoregulatory cytokine, through the vagus nerve. Methods Male aged Fischer rats (22-23-month-old) were made septic by cecal ligation and puncture (CLP) with or without dissecting the vagus nerve (vagotomy). Human ghrelin and GH or vehicle (PBS) were administrated subcutaneously at 5 h post CLP. After 20 h of CLP, serum and spleens were harvested. Results Serum TGF-beta levels were increased in septic aged rats, while ghrelin and GH treatment significantly reduced its levels. Expression of TGF-beta in the spleen was upregulated after sepsis, while ghrelin and GH treatment significantly inhibited its expression. TNF-alpha and IL-6 levels were significantly reduced after ex vivo LPS stimulation of splenocytes from rats that underwent CLP compared to sham rats; while these levels were significantly higher in splenocytes from ghrelin and GH-treated CLP rats compared to vehicle-treated CLP rats. Ghrelin and GH treatment reduced program death receptor-1 (PD-1) expression, increased human leukocyte antigen-DR (HLA-DR) expression, attenuated lymphopenia, and cleaved caspase-3 levels in the spleen of septic aged rats. Vagotomy diminished the beneficial effects of ghrelin and GH treatment in septic rats. In vitro, the addition of ghrelin, GH, or ghrelin and GH together had no effect on restoring immune response in splenocytes from CLP rats following LPS stimulation, indicating the requirement of the vagus nerve for ghrelin and GH's effect. Conclusions Ghrelin and GH attenuate immunosuppression in aged septic rats through the vagus nerve-dependent inhibition of TGF-beta production.

The adverse influences of triphenyltin (TPT) on the aquatic system have been of great concern due to their widespread use and ubiquity in water environment, although it has been prohibited as antifouling coatings. In the present study, we investigated the developmental toxicity of TPT on zebrafish embryos by exposure to different concentrations (0, 1, 10, and 100 ng/l) from 2-h post-fertilization (hpf). Some parameters of developmental abnormalities (hatching, survival, body length, and malformation) were recorded, as well as the expression of several genes involved in the retinal development and growth hormone/insulin-like growth factor (GH/IGF) axis. Our results showed that TPT exposure induced developmental toxicity, including growth inhibition, malformation, and the dysregulation of gene expression levels related to the retinal development and GH/IGF axis. Thus, our data indicated that environmental exposure of TPT could induce developmental toxicity in zebrafish embryos, and those parameters could extend our understanding of the adverse effects of TPT on aquatic organisms.