Tsilia Varvara, Uyttendaele Mieke, Kerckhof Frederiek-Maarten, Rajkovic Andreja, Heyndrickx Marc, Van de Wiele Tom
1 Laboratory of Microbial Ecology and Technology (LabMET), Department of Biochemical and Microbial Technology, Ghent University, Ghent, Belgium .
2 Laboratory of Food Microbiology and Food Preservation (LFMFP), Department of Food Safety and Food Quality, Ghent University , Ghent, Belgium .
Foodborne Pathog Dis. 2015 Nov;12(11):904-13. doi: 10.1089/fpd.2014.1926.
Adhesion of pathogenic bacteria to intestinal mucus, the protective layer of the gastrointestinal epithelium, is often considered a virulence factor. The ability of food-poisoning Bacillus cereus strains to attach to mucus and the factors affecting this interaction have not yet been investigated. Therefore, the role of adhesion in pathogenesis of B. cereus still remains unknown. In the present study, an in vitro assay based on mucin agar was used to simulate adhesion of B. cereus to mucus. Bacterial-associated factors (e.g., strain specificity and microbial competition) known to influence adhesion to different surfaces and a variety of environmental conditions (e.g., pH and oxygen) encountered in the gastrointestinal tract were investigated. The effect of these parameters on B. cereus NVH 0500/00 mucin adhesion was generally limited even in the presence of microbial competition. This suggests that B. cereus NVH 0500/00 is a versatile pathogen. Inoculation of 4 to 5 log colony-forming units (CFU) per milliliter. B. cereus NVH 0500/00 resulted in 5-6 log CFU/mL mucin-associated bacteria after a short incubation period. This indicates that this pathogenic strain could grow in the presence of mucin agar. This growth may potentially mask the effect of the studied conditions. Yet, extensive attachment of B. cereus to mucin is not necessarily a prerequisite for virulence, because other pathogenic strains do not adhere with the same efficiency to mucin. Nevertheless, adhesion may contribute to the disease by providing close contact to nutrient sources, such as mucin, which would not only result in bacterial proliferation, but also in disruption of the protective host mucus surface.
病原菌黏附于肠道黏液（胃肠道上皮的保护层）通常被视为一种毒力因子。食物中毒蜡样芽孢杆菌菌株黏附于黏液的能力以及影响这种相互作用的因素尚未得到研究。因此，黏附在蜡样芽孢杆菌发病机制中的作用仍然未知。在本研究中，基于黏蛋白琼脂的体外试验被用于模拟蜡样芽孢杆菌对黏液的黏附。研究了已知会影响对不同表面黏附的细菌相关因素（如菌株特异性和微生物竞争）以及胃肠道中遇到的各种环境条件（如pH值和氧气）。即使在存在微生物竞争的情况下，这些参数对蜡样芽孢杆菌NVH 0500/00黏蛋白黏附的影响通常也很有限。这表明蜡样芽孢杆菌NVH 0500/00是一种适应性很强的病原体。每毫升接种4至5个对数集落形成单位（CFU）的蜡样芽孢杆菌NVH 0500/00，经过短时间孵育后，导致每毫升有5 - 6个对数CFU的黏蛋白相关细菌。这表明该致病菌株能够在黏蛋白琼脂存在的情况下生长。这种生长可能会潜在地掩盖所研究条件的影响。然而，蜡样芽孢杆菌广泛黏附于黏蛋白不一定是毒力的先决条件，因为其他致病菌株对黏蛋白的黏附效率并不相同。尽管如此，黏附可能通过与营养源（如黏蛋白）紧密接触而导致疾病，这不仅会导致细菌增殖，还会破坏宿主的保护性黏液表面。
