Effects of host-associated probiotic Bacillus altitudinis B61-34b on growth performance, immune response and disease resistance of Nile tilapia (Oreochromis niloticus) raised under biofloc system

This investigation was performed to assess the influences of the host-associated probiotic Bacillus altitudinis B61-34b (BAA) on growth, immune response and disease resistance to Streptococcus agalactiae in Nile tilapia (Oreochromis niloticus). Fish (25.50 ± 0.52 g fish−1) were distributed into 15 aquaria (150 litres tank−1) at density of 20 fish tank−1. The fish were fed basal diets with BAA inclusions in different concentrations: 0 (BAA1—Control), 106 (BAA2), 107 (BAA3), 108 (BAA4) and 109 (BAA5) CFU ml−1 for 8 weeks. A completely randomized design with three replications was used. The results indicated that BAA administration generated greater (p < 0.05) skin mucus and peroxidase activities compared to the control, with maximum levels recorded in BAA4 and BAA5. Higher serum immunities, such as serum lysozyme, serum peroxidase, complement, phagocytosis and respiratory burst activities were observed in the BAA4 and BAA5 dietary groups compared to the control, BAA1, BAA2 and BAA3 diets. The relative percentage of survival, growth performance and FCR were also significantly higher (p < 0.05) in the BAA4 and BAA5 groups. In conclusion, dietary supplementation of B. altitudinis at 108 CFU ml−1 can improve Nile tilapia's growth performance, skin mucus and serum immunities, and disease resistance

KLF4 is a novel regulator of the constitutively expressed HSP90

Krüppel-like factor 4 (KLF4) is a zinc finger-containing transcription factor with diverse regulatory functions in cell growth, proliferation, and differentiation. But little is known about the regulation of KLF4 on the expression of HSP90 (HSP84 and HSP86). In the current study, overexpression of KLF4 was firstly identified to promote the basal expression of HSP90 (HSP84 and HSP86) but not the inducible expression in the C2C12 cells and RAW264.7 cells. Conversely, KLF4 inhibition by antisense oligonucleotides markedly decreased the constitutive expression of HSP90 (HSP84 and HSP86). Here, we also presented data that overexpression of KLF4 resulted in enhanced promoter activities of HSP84. Consistently, KLF4 bind to the KLF4 binding sites in the promoter regions of HSP84 directly. Together, these findings support a role for KLF4 as a novel regulator of the constitutive expression of HSP90

Increased stability of Bcl-2 in HSP70-mediated protection against apoptosis induced by oxidative stress

We have previously shown that heat shock protein 70 (HSP70) markedly inhibits H2O2-induced apoptosis in mouse C2C12 myogenic cells by reducing the release of Smac. However, the molecular mechanism by which HSP70 interferes with Smac release during oxidative stress-induced apoptosis is not understood. In the current study, we showed that HSP70 increased the stability of Bcl-2 during oxidative stress. An antisense phosphorothioate oligonucleotide against Bcl-2 caused selective inhibition of Bcl-2 protein expression induced by HSP70 and significantly attenuated HSP70-mediated cell protection against H2O2-induced release of Smac and apoptosis. Taken together, our results indicate that there are important relationships among HSP70, Bcl-2, release of Smac, and induction of apoptosis by oxidative stress