Departamento de Microbiologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.
Laboratório de Entomologia Médica, Instituto René Rachou, Fiocruz, Belo Horizonte, MG, Brazil.
J Med Microbiol. 2012 Sep;61(Pt 9):1194-1207. doi: 10.1099/jmm.0.042283-0. Epub 2012 May 11.
Recently, much attention has been given to the use of probiotics as an adjuvant for the prevention or treatment of gastrointestinal pathology. The great advantage of therapy with probiotics is that they have few side effects such as selection of resistant bacteria or disturbance of the intestinal microbiota, which occur when antibiotics are used. Adhesion of pathogenic bacteria onto the surface of probiotics instead of onto intestinal receptors could explain part of the probiotic effect. Thus, this study evaluated the adhesion of pathogenic bacteria onto the cell wall of Saccharomyces boulardii and Saccharomyces cerevisiae strains UFMG 905, W303 and BY4741. To understand the mechanism of adhesion of pathogens to yeast, cell-wall mutants of the parental strain of Saccharomyces cerevisiae BY4741 were used because of the difficulty of mutating polyploid yeast, as is the case for Saccharomyces cerevisiae and Saccharomyces boulardii. The tests of adhesion showed that, among 11 enteropathogenic bacteria tested, only Escherichia coli, Salmonella Typhimurium and Salmonella Typhi adhered to the surface of Saccharomyces boulardii, Saccharomyces cerevisiae UFMG 905 and Saccharomyces cerevisiae BY4741. The presence of mannose, and to some extent bile salts, inhibited this adhesion, which was not dependent on yeast viability. Among 44 cell-wall mutants of Saccharomyces cerevisiae BY4741, five lost the ability to fix the bacteria. Electron microscopy showed that the phenomenon of yeast-bacteria adhesion occurred both in vitro and in vivo (in the digestive tract of dixenic mice). In conclusion, some pathogenic bacteria were captured on the surface of Saccharomyces boulardii, Saccharomyces cerevisiae UFMG 905 and Saccharomyces cerevisiae BY4741, thus preventing their adhesion to specific receptors on the intestinal epithelium and their subsequent invasion of the host.
最近，人们越来越关注益生菌作为预防或治疗胃肠道病理的辅助手段的应用。益生菌治疗的一个很大的优势是它们几乎没有副作用，例如当使用抗生素时会出现选择耐药菌或干扰肠道微生物群的情况。致病菌黏附在益生菌表面而不是黏附在肠道受体上，可以解释益生菌部分作用的机制。因此，本研究评估了致病菌黏附到酿酒酵母和酿酒酵母 UFMG 905、W303 和 BY4741 菌株细胞壁上的情况。为了了解病原体黏附到酵母上的机制，使用了酿酒酵母亲本菌株 BY4741 的细胞壁突变体，因为多倍体酵母（如酿酒酵母和布拉氏酵母）的突变很困难。黏附试验表明，在测试的 11 种肠道致病菌中，只有大肠杆菌、鼠伤寒沙门氏菌和伤寒沙门氏菌黏附到布拉氏酵母、酿酒酵母 UFMG 905 和酿酒酵母 BY4741 的表面。甘露糖的存在，在一定程度上胆汁盐的存在，抑制了这种黏附，而这种黏附不依赖于酵母的活力。在酿酒酵母 BY4741 的 44 个细胞壁突变体中，有 5 个失去了固定细菌的能力。电子显微镜显示，酵母-细菌黏附现象既发生在体外，也发生在体内（在双栖小鼠的消化道中）。总之，一些致病菌被捕获在布拉氏酵母、酿酒酵母 UFMG 905 和酿酒酵母 BY4741 的表面，从而防止它们黏附在肠上皮的特定受体上，并随后入侵宿主。
