Magic™ Anti-GABA polyclonal antibody

EnterotoxigenicEscherichia coli(ETEC) infection is the most common cause of diarrhea in piglets, and ETEC could increase intestinal gamma-aminobutyric acid (GABA)-producing bacteria to affect intestinal immunity. However, the effect of GABA on ETEC-infected piglets is still unclear. This study aims at investigating the impact of dietary GABA supplementation on the growth performance, diarrhea, intestinal morphology, serum amino acid profile, intestinal immunity, and microbiota in the ETEC-infected piglet model. Eighteen piglets were randomly divided into two groups, in which the piglets were fed with a basal diet with 20 mg kg(-1)GABA supplementation or not. The experiment lasted for three weeks, and the piglets were challenged with ETEC K88 on the fifteenth day. The results showed that dietary GABA reduced the feed conversion ratio, promoted the kidney organ index but did not affect the diarrheal score and small intestinal morphology in ETEC-challenged piglets. Ileal mucosal amino acids (such as carnosine and anserine) and serum amino acids (including threonine and GABA) were increased upon GABA supplementation. GABA enhanced ileal gene expression of TNF-alpha, IFN-gamma, pIgR, and MUC2, while inhibited the ileal expression of IL-18 in ETEC-challenged piglets. GABA supplementation also highly regulated the intestinal microbiota by promoting community richness and diversity and reducing the abundance of the dominant microbial population of the ileal microbiota. Collectively, GABA improves growth performance, regulates the serum amino acid profile, intestinal immunity, and gut microbiota in ETEC-challenged piglets. This study is a fine attempt to reveal the function of GABA in ETEC-infected piglets. It would contribute to the understanding of the roles of exogenous nutrition on the host response to ETEC infection.

Follistatin-like 1 (FSTL1), also named transforming growth factor (TGF)-beta 1-inducible gene, is a secreted extracellular glycoprotein expressing widely in nervous system. Several recent studies have revealed that FSTL1 plays an essential role in neurological diseases including neuropathic pain and ischemic stroke. It proves that FSTL1 suppresses synaptic transmission by activating Na/K-ATPase in DRG neurons and inhibits neuronal apoptosis by phosphorylation AKT signaling. However, it is not clear whether FSTL1 can play a role in other type of neuron or neurodegenerative diseases. In this study, we found that the mice with Fstl1 genetic knockdown showed not only the impairments of learning and memory abilities, but also abnormal neural oscillations and synaptic plasticity in the hippocampus. Subsequently, we identified broad transcriptional changes including 55 up-regulated and 184 down-regulated genes in Fstl1 knockdown mice by RNA-Seq analysis, as well as neurotransmitter transport, synaptic transmission and disease-related genes. The expression changes of some DEGs were further validated via quantitative Realtime PCR (qRT-PCR). Further patch-clamp whole cell recording showed that Fstl1(+/-) mice displayed a significant decrease in glutamatergic synaptic transmission and increase in GABAergic synaptic transmission, which were consistent with the RNA-Seq analysis. Taken together, our results provide an evidence and a possibly underlying mechanism for the critical role of FSTL1 in the hippocampus on learning and memory and normal neural oscillations, suggesting that FSTL1 may plays an important role in neurodegenerative diseases related to cognitive impairments.