Introduction

Polymicrobial biofilms have a significant impact on pathogenesis of infectious microorganisms. Many human diseases are affected by colonization of multi-species communities affecting negatively the treatments and increase the risks for the health. In particular, in the epithelium of the stomach co-existence between C. albicans and H. pylori has been described, which has been associated to a synergistic effect on ulcer pathogenesis.

Objective

The objective of this work was to advance in the understanding of surface interaction between H. pylori and C. albicans for the formation of polymicrobial biofilms.

Methods

Studies of microbial surfaces both bacterium, yeast and co-cultures of them were carried out by infrared spectroscopy, deconvolution analysis, transmission and scanning electron microscopies, and optic microscopy. Additional methods were used to contrast the results as dynamic light scattering, contact angle, agarose gel electrophoresis and gene amplification.

Results

Several surface interaction mechanisms promote the anchoring of H. pylori on C. albicans, cell co-aggregation, and polymicrobial biofilm formation, main identified interactions were: (i) hydrophobic interactions between non-polar peptide chains and lipid structures, characterized by θ_w among 84.9 ± 1.6 (γ = 22.78 mJ/m² with 95.3 of dispersive contribution) and 76.6 ± 3.8 (γ = 17.34 mJ/m², 40.2 of dispersive contribution) for C. albicans and H. pylori, respectively, (ii) hydrogen bonds between surface components of yeast and bacterium (e.g., SH⋅⋅⋅NH₂ or SH⋅⋅⋅OCO) and (iii) thiol-mediated surface interactions identified by displacements to lower wavenumbers (Δv = 5 cm⁻¹). Evidence of internalization and electrostatic interactions were not evidenced. All observations were congruent with the biofilm formation, including the identification of small-size biostructures (i.e., 122–459 nm) associated with extracellular proteins, extracellular DNA, or outer membrane vesicles were observed characteristic of biofilm formation.

Conclusion

It is concluded that biofilm is formed by co-aggregation after anchoring of H. pylori on C. albicans. Several surface interactions were associated with the prevalence of H. pylori, the possibility to find C. albicans in the stomach epithelium infected by H. pylori, but also, strength interactions could be interfering in experimental observations associated with bacterial-DNA detection in culture mixtures.

中文翻译：

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多种表面相互作用机制指导白色念珠菌和幽门螺杆菌之间双物种生物膜的锚定、共聚集和形成

介绍

多微生物生物膜对传染性微生物的发病机制具有重要影响。许多人类疾病受到多物种群落殖民化的影响，对治疗产生负面影响并增加健康风险。特别是，在胃的上皮细胞中，白色念珠菌和幽门螺杆菌共存，这与溃疡发病机制的协同作用有关。

客观的

这项工作的目的是促进对幽门螺杆菌和白色念珠菌之间的表面相互作用的理解，以形成多微生物生物膜。

方法

通过红外光谱、反卷积分析、透射和扫描电子显微镜以及光学显微镜对细菌、酵母及其共培养物的微生物表面进行了研究。其他方法用于对比结果，如动态光散射、接触角、琼脂糖凝胶电泳和基因扩增。

结果

几种表面相互作用机制促进H. pylori在白色念珠菌上的锚定、细胞共聚集和多微生物生物膜的形成，主要确定的相互作用是：(i) 非极性肽链和脂质结构之间的疏水相互作用，以θ _w为特征白色念珠菌和幽门螺杆菌分别为84.9 ± 1.6（γ = 22.78 mJ/m ²，色散贡献为 95.3）和 76.6 ± 3.8（γ = 17.34 mJ/m ²，色散贡献为 40.2） ，（ii）酵母和细菌表面成分之间的氢键（例如，S H⋅⋅⋅NH ₂或S H⋅⋅⋅OCO ) 和 (iii) 硫醇介导的表面相互作用，通过位移识别到较低的波数 (Δ v  = 5 cm ^-1 )。没有证据表明内化和静电相互作用。所有观察结果与生物膜形成一致，包括与细胞外蛋白质、细胞外 DNA 或外膜囊泡相关的小尺寸生物结构（即 122-459 nm）的鉴定，观察到生物膜形成的特征。

结论

得出的结论是，生物膜是由幽门螺杆菌锚定在白色念珠菌上后共聚集形成的。几种表面相互作用与 H. pylori 的流行有关，在H. pylori感染的胃上皮中发现C. albicans的可能性，而且，强度相互作用可能会干扰与培养混合物中细菌 DNA 检测相关的实验观察.