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65 Exploring molecular mechanisms behind Lactobacillus protection offered to Caenorhabditis elegans: the role of neurotransmitters

生物 秀丽隐杆线虫 突变体 沙门氏菌 多巴胺 微生物学 细胞生物学 遗传学 细菌 基因 神经科学
作者
Linyan Li,Xiaozhen Liu,Leming Jiang,Hai Yu,Shaoping Nie,Mingyong Xie,Joshua Gong
出处
期刊:Journal of Animal Science [Oxford University Press]
卷期号:98 (Supplement_4): 40-41
标识
DOI:10.1093/jas/skaa278.073
摘要

Abstract Lactobacillus are commonly used as probiotics in livestock production to improve animal gut health and performance. We previously reported the selection of Lactobacillus zeae LB1, which was able to reduce Salmonella infection in chickens and pigs, through the life-span assay of Caenorhabditis elegans infected with Salmonella Typhimurium DT104. To understand the molecular mechanisms behind the probiotic effect, the present study used C. elegans as a model to investigate the influence of LB1 on the behavior plasticity and roles of both serotonin and dopamine in C. elegans responding to Salmonella infection and LB1 protection. Pre-exposure to LB1 did not elicit aversive olfactory behavior of both the wild-type nematode (N2) and mutants defective in serotonin (tph-1) or dopamine (cat-2) production towards DT104, although LB1 was much more attractive than DT104 to C. elegans. Life-span studies showed that both the mutants succumbed faster than N2 to DT104 infection. Pre-exposure to LB1 significantly increased the survival level of both N2 and mutant tph-1. However, LB1 provided no protection to mutant cat-2. Supplementation of dopamine restored both the resistance of mutant cat-2 to Salmonella infection and the protection from LB1 to mutant cat-2. These results suggest that both serotonin and dopamine have a role in the host defense of C. elegans to Salmonella infection, and that the LB1 protection effect was not dependent on modifying olfactory preference of the nematode, but mediated by dopamine. Additionally, the p38-mitogen activated protein kinase signaling and IGFR-1/DAF-16 signaling pathways may have also participated in the protection under dopamine regulation.

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