Investigation of ptsG gene in response to xylose utilization in Corynebacterium glutamicum.

Corynebacterium glutamicum strains NC-2 were able to grow on xylose as sole carbon sources in our previous work. Nevertheless, it exhibited the major shortcoming that the xylose consumption was repressed in the presence of glucose. So far, regarding C. glutamicum, there are a number of reports on ptsG gene, the glucose-specific transporter, involved in glucose metabolism. Recently, we found ptsG had influence on xylose utilization and investigated the ptsG gene in response to xylose utilization in C. glutamicum with the aim to improve xylose consumption and simultaneously utilized glucose and xylose. The ptsG-deficient mutant could grow on xylose, while exhibiting noticeably reduced growth on xylose as sole carbon source. A mutant deficient in ptsH, a general PTS gene, exhibited a similar phenomenon. When complementing ptsG gene, the mutant ΔptsG-ptsG restored the ability to grow on xylose similarly to NC-2. These indicate that ptsG gene is not only essential for metabolism on glucose but also important in xylose utilization. A ptsG-overexpressing recombinant strain could not accelerate glucose or xylose metabolism. When strains were aerobically cultured in a sugar mixture of glucose and xylose, glucose and xylose could not be utilized simultaneously. Interestingly, the ΔptsG strain could co-utilize glucose and xylose under oxygen-deprived conditions, though the consumption rate of glucose and xylose dramatically declined. It was the first report of ptsG gene in response to xylose utilization in C. glutamicum.

Extracellular polysaccharide from Bacillus sp. strain LBP32 prevents LPS-induced inflammation in RAW 264.7 macrophages by inhibiting NF-κB and MAPKs activation and ROS production.

Extracellular polysaccharides (EPSs) are high-molecular weight sugar-based polymers that are synthesized and secreted by many microorganisms. Recently, EPSs have attracted particular attention due to their multiple biological functions including anti-inflammation. However, studies rarely reported the molecular mechanisms underlying their functions. We previously purified an EPS from an oligotrophic bacteria (Bacillus sp. LBP32) found in Lop Nur Desert, which possesses a potent antioxidant activity, while the anti-inflammatory effects of EPS and signaling mechanisms underlying its action have not been clarified. In this study, we demonstrated that EPS significantly inhibited the LPS-induced release of pro-inflammatory mediators, such as nitric oxide (NO), IL-6 and TNF-α, without any significant cytotoxicity. EPS also downregulated the expression of nitric oxide synthase (iNOS) induced by LPS. Furthermore, activation of nuclear factor κB (NF-κB) was abrogated by EPS through inhibited the phosphorylation of IκB kinase (IKK). Activations of Mitogen-activated protein kinases (MAPKs), including p38 MAPK and c-Jun N-terminal kinase (JNK), were also found to be inhibited by EPS. In addition, the level of intracellular reactive oxygen species (ROS) was also significantly decreased with the treatment of EPS. In vivo experiments were conducted and showed that EPS could greatly improve the outcome of mice with LPS-induced endotoxic shock. Taken together, our data indicate that EPS prevents LPS-induced inflammatory response by inhibiting NF-κB and MAPKs activation and ROS production.