Delpech Pierre, Rifa Etienne, Ball Graham, Nidelet Sabine, Dubois Emeric, Gagne Geneviève, Montel Marie-Christine, Delbès Céline, Bornes Stéphanie
Université Clermont Auvergne, INRA, UMRF Aurillac, France.
John van Geest Cancer Research Centre, School of Science and Technology, Nottingham Trent University Nottingham, UK.
Front Microbiol. 2017 Mar 8;8:359. doi: 10.3389/fmicb.2017.00359. eCollection 2017.
The bio-preservation potential of lies in its capacity to inhibit the growth of , especially , in dairy products and . , inhibition is modulated by the level of aeration, owing to hydrogen peroxide (HO) production by under aeration. The response to this inhibition has already been studied. However, the molecular mechanisms of underlying the antagonism against have never been explored. This study provides evidence of the presence of another extracellular inhibition effector . This effector was neither a protein, nor a lipid, nor a polysaccharide, nor related to an L-threonine deficiency. To better understand the HO-related inhibition mechanism at the transcriptome level and to identify other mechanisms potentially involved, we used RNA sequencing to determine the transcriptome response of to different aeration levels and to the presence or absence of . The transcriptome differed radically between different aeration levels mainly in biological processes related to fundamental functions and nutritional adaptation. The transcriptomic response of to aeration level differed according to the presence or absence of . The higher concentration of HO with high aeration was not associated with a higher expression of HO-synthesis genes (, , and ) but rather with a repression of HO-degradation genes (, , , and ). We showed that displayed an original, previously undiscovered, HO production regulation mechanism among bacteria. In addition to the key factor HO, the involvement of another extracellular effector in the antagonism against was shown. Future studies should explore the relation between HO-metabolism, HO-producing LAB and the pathogen they inhibit. The nature of the other extracellular effector should also be determined.
[具体名称]的生物保鲜潜力在于其抑制乳制品和[具体产品]中[具体微生物名称]生长的能力，尤其是[具体微生物名称]。[具体微生物名称]的抑制作用受通气水平调节，这是因为[具体微生物名称]在通气条件下会产生过氧化氢（H₂O₂）。此前已对[具体微生物名称]对这种抑制作用的反应进行了研究。然而，[具体微生物名称]对抗[具体微生物名称]的拮抗作用背后的分子机制从未被探索过。本研究提供了另一种细胞外抑制效应物存在的证据。这种效应物既不是蛋白质，也不是脂质，也不是多糖，也与L-苏氨酸缺乏无关。为了在转录组水平上更好地理解与H₂O₂相关的抑制机制，并确定可能涉及的其他机制，我们使用RNA测序来确定[具体微生物名称]对不同通气水平以及[具体微生物名称]存在与否的转录组反应。不同通气水平下[具体微生物名称]的转录组在与基本功能和营养适应相关的生物学过程中存在根本差异。[具体微生物名称]对通气水平的转录组反应因[具体微生物名称]的存在与否而有所不同。高通气条件下较高浓度的H₂O₂与[具体微生物名称]H₂O₂合成基因（[具体基因名称1]、[具体基因名称2]和[具体基因名称3]）的较高表达无关，而是与[具体微生物名称]H₂O₂降解基因（[具体基因名称4]、[具体基因名称5]、[具体基因名称6]和[具体基因名称7]）的抑制有关。我们表明，[具体微生物名称]在细菌中表现出一种独特的、以前未被发现的H₂O₂产生调节机制。除了关键因子H₂O₂外，还显示了另一种细胞外效应物参与了对[具体微生物名称]的拮抗作用。未来的研究应探索H₂O₂代谢、产生H₂O₂的乳酸菌与其抑制的病原体之间的关系。还应确定另一种细胞外效应物的性质。
