Indeed, we observed a lack of adherence between phESC derivates, resulting in poor sphere forming capability, and poor adherence to surfaces.
Some have been proved to involve the pathogenicity [39], [40], while some were found to serve a structural role benefitting the bacterium by providing protection from antimicrobial agents and host defenses [16], [41] [43], helping nutrient acquisition [44], or promoting adherence to surfaces [45] [47] and biofilm formation [17], [48].
This suggests that adherence to surface-associated MUC5B may have 'primed' the cells allowing them to respond to the presence of MUC5B in the fluid phase.
These findings are concordant with observations on surface adhesion (greater invasive capacity and less adherence to surfaces).
Bacterial adherence to surfaces is one of the initial steps leading to biofilm formation and is therefore a significant microbiological event in medicine and the environment [ 17, 18].
Several groups have found that P-fimbriae-mediated adherence to surfaces by E. coli is reduced by A-type PACs [ 6, 48].
These proteins self-assemble in the form of an insoluble amphipathic membrane at hydrophobic/hydrophilic interfaces, thereby forming protective surface coatings of fungal structures and aiding in their adherence to surfaces.
Well-studied EPS in other bacteria, such as in Pseudomonas aeruginosa, have several roles in pathogenicity; EPS contributes to biofilm formation, adherence to surfaces and host cells, evasion of phagocytosis, and elicitation of immune response [ 32- 34].
Several reports have shown that indole acts as a signalling molecule in E. coli to: 1) prepare cells for a nutrient-poor environment and increase catabolism of amino acids, 2) up-regulate genes that encode drug exporters (e.g. acrDE, mdtAE, cusB) to increase bacterial tolerance to toxic compounds, 3) increase bacterial adherence to surfaces, and 4) delay cell division [ 81- 84].
