[Key technology for anaerobic fermentation of L-alanine and its commercialization].

Traditionally, amino acids are produced mainly by chemical synthesis or aerobic fermentation. Compared to chemical synthesis, production of amino acids by microbial fermentation directly uses renewable resources as feedstock and this reduces the dependence on petroleum-based compounds and decreases pollutants generation and toxic substrates usage. Fermentation under aerobic conditions has been used widely for its fast growth and high titers. However, a large amount of carbon is used for cell growth and this results in high biomass but low yield of target chemicals. Unlike the long history of aerobic fermentation, the commercial production of amino acids by anaerobic fermentation is realized only in recent years. It has several advantages such as simpler operation, no need for oxygen supply, and high yield close to the theoretical maximum value. L-alanine is the first amino acid commercially produced by anaerobic fermentation. In this article, we summarize the key technology for anaerobic fermentative production of L-alanine and its commercialization. As it is shown to be low-cost, high-efficiency, and environmental-friendly, anaerobic fermentation is expected to be widely used in industrial process and brings greater economic values and social benefits in the future.

VSIG4 alleviates intracerebral hemorrhage induced brain injury by suppressing TLR4-regulated inflammatory response.

AIMS: Numerous evidence demonstrated that macrophage mediated inflammation contributed to brain injury following ICH, but the molecular mechanism had not been well studied. V-set immunoglobulin-domain-containing 4 (VSIG4), specifically expresses in resting tissue-resident macrophages, can deliver anti-inflammatory signals into various inflammatory diseases. However, the role of VSIG4 on ICH has not been reported. METHODS: In the present study, we investigated the levels of VSIG4 in macrophages following ICH. Furthermore, Macrophage M1/M2 polarization, pro-inflammatory cytokine production, BBB disruption, brain water content and neurological function were examined in ICH mice. In addition, TLR4/NF-κß downstream signals were also analyzed. RESULTS: The results showed that VSIG4 levels of macrophage decreased following ICH, leading to macrophage M1 polarization. Up-regulation of VSIG4 inhibited macrophage M1 polarization, pro-inflammatory cytokine production, BBB disruption, as well as neurological deficits. Up-regulation of VSIG4 attenuated macrophage TLR4 levels following ICH. Co-IP demonstrated that VSIG4 could interact with TLR4 and inhibit its expression. CONCLUSIONS: Our data demonstrated that VSIG4 was negatively correlated with TLR4 and involved in the pathogenesis of ICH, which prevented brain injury and attenuated deleterious inflammatory responses following ICH. In addition, the anti-inflammatory effect of VSIG4 was mainly through the blockage of TLR4/NF-κß signaling.