Transcriptomic and metabolomic insights into the antimicrobial effect of Leuconostoc mesenteroides or lactic acid on pathogenic Gallibacterium anatis

Author:

Zhang Hua1,HuangFu HePing2,Qin GuangYong1,Wu GuoFang3,Wang Lei3,Tan ZhongFang1

Affiliation:

1. Zhengzhou University

2. Henan University of Animal Husbandry and Economy

3. Qinghai University

Abstract

Abstract Gallibacterium anatis (G. anatis) is an opportunistic poultry pathogen that poses a threat to human health via food chain and can also lead to great economic loss in poultry industries. Our previous studies have demonstrated that the lactic acid producing bacteria Leuconostoc mesenteroides QZ1178 can effectively inhibit the growth of G. anatis by acid production whereas the mechanism is unclear. The current research intended to further probe the molecular mechanism underlying this acid induced antimicrobial effect. The TEM results showed that the cell membrane of G. anatis (GAC026) was damaged and cells were even lysed in the presence of cell free supernatants from Leuconostoc mesenteroides (CFS) or lactic acid. Lactic acid showed more antimicrobial effect than CFS. In this study, the changes in the transcriptome and the metabolic profile of G. anatis under acid stress at different stages have been studied. Using culture medium added with CFS (pH 3.6) or lactic acid (pH 3.6) at 1:1 ratio, 677 differentially transcribed genes and 374 metabolites were detected in G. anatis. The interaction network of all identified differentially expressed genes and metabolites was constructed to outline the potential regulatory genes and dominant pathways in response to acid stress. The results of real-time reverse transcription quantitative PCR (RT-qPCR) further confirmed the results of the transcriptomic analyses. Typically, citrate, lactic acid, L-malic acid, and oxaloacetate were reduced by acid stress in G. anatis, which suggested that lactic acid greatly disturbed energy metabolism. Overall, this work provides comprehensive understanding of stress response and cell death of G. anatis by lactic acid.

Publisher

Research Square Platform LLC

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