Abstract
Cell‐to‐cell early contact between pathogens and their host cells is required for the establishment of many infections. Among various surface factors produced by bacteria that allow an organism to become established in a host, the class of adhesins is a primary determinant. Burkholderia cenocepacia adheres to the respiratory epithelium of cystic fibrosis patients and causes chronic inflammation and disease. Cell‐to‐cell contacts are promoted by various kinds of adhesins, including trimeric autotransporter adhesins (TAAs). We observed that among the 7 TAA genes found in the B. cenocepacia K56‐2 genome, two of them (BCAM2418 and BCAS0236) express higher levels of mRNA following physical contact with host cells. Further analysis revealed that the B. cenocepacia K56‐2 BCAM2418 gene shows an on–off switch after an initial colonization period, exhibits a strong expression dependent on the host cell type, and enhances its function on cell adhesion. Furthermore, our analysis revealed that adhesion to mucin‐coated surfaces dramatically increases the expression levels of BCAM2418. Abrogation of mucin O‐glycans turns BCAM2418 gene expression off and impairs bacterial adherence. Overall, our findings suggest that glycosylated extracellular components of host membrane might be a binding site for B. cenocepacia and a signal for the differential expression of the TAA gene BCAM2418.
Highlights
Bacterial initial contact to host cells has been defined as a crucial step in the overall host–pathogen interaction process (Pizarro-Cerdá & Cossart, 2006)
The results described above reveal that B. cenocepacia K56-2 can sense the environment through promoting a specific interaction with mucins which thereby triggers the expression of the BCAM2418 gene
We found that the pretreatment of mucins with the O-glycosidase enzyme can effectively reduce bacterial adhesion (Figure 6b). These results indicate that B. cenocepacia K56-2 binds to mucins by mediating recognition to the O-glycans attached to the external mucin surface
Summary
Bacterial initial contact to host cells has been defined as a crucial step in the overall host–pathogen interaction process (Pizarro-Cerdá & Cossart, 2006). It has been described that the sense and adherence of the bacteria to the host could lead to a prompt transcription modulation of a panel of virulence-associated genes, adhesive molecules, surface antigens, and toxins (Alsharif, Ahmad, Shah, Busby, & Krachler, 2015; Kansal et al, 2013; Katsowich et al, 2017). These physiological alterations can result in a more robust bacterial. This study defines the behavior of the TAAs during the step of bacterial adhesion and provide insights aiming to determine potential targets for therapeutic proposals
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