Sicard Jean-Félix, Vogeleer Philippe, Le Bihan Guillaume, Rodriguez Olivera Yaindrys, Beaudry Francis, Jacques Mario, Harel Josée
1Groupe de Recherche sur les Maladies Infectieuses en Production Animale, Centre de Recherche en Infectiologie Porcine et Avicole, Faculté de Médecine Vétérinaire, Université de Montréal, St-Hyacinthe, QC J2S 2M2 Canada.
2Regroupement de Recherche Pour un Lait de Qualité Optimale (Op+Lait), Faculté de Médecine Vétérinaire, Université de Montréal, Saint-Hyacinthe, QC J2S 2M2 Canada.
Gut Pathog. 2018 Jun 22;10:26. doi: 10.1186/s13099-018-0252-y. eCollection 2018.
The intestinal mucous layer is a physical barrier that limits the contact between bacteria and host epithelial cells. There is growing evidence that microbiota-produced metabolites can also be specifically sensed by gut pathogens as signals to induce or repress virulence genes. Many , including adherent and invasive (AIEC) strains, can form biofilm. This property can promote their intestinal colonization and resistance to immune mechanisms. We sought to evaluate the impact of mucus-derived sugars on biofilm formation of .
We showed that the mucin sugar -acetyl-glucosamine (NAG) can reduce biofilm formation of AIEC strain LF82. We demonstrated that the inactivation of the regulatory protein NagC, by addition of NAG or by mutation of gene, reduced the biofilm formation of LF82 in static condition. Interestingly, real-time monitoring of biofilm formation of LF82 using microfluidic system showed that the mutation of impairs the early process of biofilm development of LF82. Thus, NAG sensor NagC is involved in the early steps of biofilm formation of AIEC strain LF82 under both static and dynamic conditions. Its implication is partly due to the activation of type 1 fimbriae. NAG can also influence biofilm formation of other intestinal strains.
This study highlights how catabolism can be involved in biofilm formation of . Mucus-derived sugars can influence virulence properties of pathogenic and this study will help us better understand the mechanisms used to prevent colonization of the intestinal mucosa by pathogens.
肠道黏液层是一种物理屏障,可限制细菌与宿主上皮细胞之间的接触。越来越多的证据表明,微生物群产生的代谢物也可被肠道病原体特异性感知为诱导或抑制毒力基因的信号。许多细菌,包括黏附和侵袭性(AIEC)菌株,都能形成生物膜。这种特性可促进它们在肠道内的定植以及对免疫机制的抵抗。我们试图评估黏液衍生糖对AIEC生物膜形成的影响。
我们发现黏蛋白糖N-乙酰葡糖胺(NAG)可减少AIEC菌株LF82的生物膜形成。我们证明,通过添加NAG或通过nagC基因突变使调节蛋白NagC失活,可降低LF82在静态条件下的生物膜形成。有趣的是,使用微流控系统对LF82生物膜形成进行实时监测表明,nagC突变会损害LF82生物膜发育的早期过程。因此,NAG传感器NagC在静态和动态条件下均参与AIEC菌株LF82生物膜形成的早期步骤。其作用部分归因于1型菌毛的激活。NAG还可影响其他肠道细菌菌株的生物膜形成。
本研究突出了分解代谢如何参与细菌的生物膜形成。黏液衍生糖可影响致病性细菌的毒力特性,这项研究将有助于我们更好地理解用于防止病原体在肠道黏膜定植的机制。