Selenium deficiency induces splenic growth retardation by deactivating the IGF-1R/PI3K/Akt/mTOR pathway.

Selenium (Se) deficiency impairs the development and function of immune system in human beings and animals. We investigated the effect and molecular mechanism of Se deficiency on spleen development in chicken. The concentration of Se in blood and spleen, the spleen weight and splenocyte number, the histological characteristics of spleen, the concentration of growth factors in serum, the transcription level of growth factor receptor gene and the activity of growth and proliferation pathway in spleen were investigated. We found that the growth of the spleen and the splenocyte number were significantly lower in the chicken fed with Se-deficient diet for 21 and 35 days. The ELISA and qRT-PCR results showed that the serum IGF-I concentration and the transcription level of IGF1R gene in spleen were significantly lower in the SD group. The Western blotting and immunohistochemistry results showed that Se deficiency could deactivate the PI3K/Akt/mTOR pathway in spleen. In summary, the results indicated that Se deficiency decreases the growth rate of spleen and the number of splenic lymphocytes by deactivating the IGF-1R/PI3K/Akt/mTOR pathway.

Selenium deficiency induces duodenal villi cell apoptosis via an oxidative stress-induced mitochondrial apoptosis pathway and an inflammatory signaling-induced death receptor pathway.

Selenium (Se) is an important nutritional trace element possessing antioxidant properties. Our goal was to elucidate the effect and mechanism of Se deficiency on the intestinal cell fate. One-day-old three-yellow chickens were fed a low Se diet for 1, 3, and 5 weeks. Histologic characteristics, protein expression profiles, antioxidant activities, inflammatory signaling, and the apoptosis status in duodenum mucosa were investigated. Histological results showed that Se deficiency could increase inflammatory cell infiltration, karyopyknosis of the epithelial cells, cytoplasm vacuolization and dissolution of goblet cells. The proteomics results indicated that Se deficiency could induce apoptosis of cells in duodenal villi via inhibition of antioxidant redox signaling and activation of NF-κB signaling. Further analysis results showed that Se deficiency decreased the total antioxidant capacity of duodenum mucosa via down-regulating the transcription level and activities of glutathione peroxidase (GPX), reduced glutathione (GSH), and thioredoxin reductase (TrxR). The NF-κB signaling pathway was activated by Se deficiency-induced reactive oxygen species (ROS). TUNEL, DNA ladder, immunohistochemical assay, and western blotting proved that selenium deficiency could induce duodenal villi cell apoptosis. The results also indicated that Se deficiency can cause duodenal villi cell apoptosis via an oxidative stress-induced mitochondrial apoptosis pathway (intrinsic pathway) and an inflammatory signaling-induced death receptor pathway (extrinsic pathway). Our data may provide new insight into the prevention and treatment of chronic diarrhea caused by Se deficiency.

Low-level laser therapy attenuates LPS-induced rats mastitis by inhibiting polymorphonuclear neutrophil adhesion.

The aim of this study was to investigate the effects of low-level laser therapy (LLLT) on a rat model of lipopolysaccharide (LPS)-induced mastitis and its underlying molecular mechanisms. The rat model of mastitis was induced by inoculation of LPS through the canals of the mammary gland. The results showed that LPS-induced secretion of IL-1ß and IL-8 significantly decreased after LLLT (650 nm, 2.5 mW, 30 mW/cm(2)). LLLT also inhibited intercellular adhesion molecule-1 (ICAM-1) expression and attenuated the LPS-induced decrease of the expression of CD62L and increase of the expression of CD11b. Moreover, LLLT also suppressed LPS-induced polymorphonuclear neutrophils (PMNs) entering the alveoli of the mammary gland. The number of PMNs in the mammary alveolus and the myeloperoxidase (MPO) activity were decreased after LLLT. These results suggested that LLLT therapy is beneficial in decreasing the somatic cell count and improving milk nutritional quality in cows with an intramammary infection.