Bacterial docking and anchoring to the heart!

I apologise but I cannot indeed remember where exactly I saw this presentation slide for the first time (probably here), so I cannot refer back to the web document I got it from. But I was most intrigued about the concepts of docking and anchoring of bacteria to eukaryotic cells. Concepts I was partially unaware of on its biomolecular nature, but had a mild understanding of what could actually mean physically.

Bacterial adhesion can occur in two major ways:

In a basic primary fashion known as the docking stage and by secondary means known as locking or anchoring.

Docking is reversible and occurs between the bacterial cell surface and the surface of interest where electrostatic and hydrophobic interactions play a role [1].

Anchoring becomes irreversible if no prompt intervention takes place, and involves molecularly-mediated binding between specific adhesins and the compromised surface. This compromised agent subjected to an initial locking will become susceptible to a different range of adhering organisms, thus allowing a pluralised matrix to form in the shape of a biofilm varying in strain identities [1].

Both can lead to serious defense suppression, but the second can get the host death compromised by adding to antimicrobial drug resistance by compromising the glycocalyx (image below).

 [2]

The glycocalyx is a carbohidrate-enriched layer surrounding the outside of many eukaryotic and also prokaryotic cells. It basically reports on the health state of a cell and its disruption means disease! Especially in hyperglycemic subjects, thus diabetic patients are prone to loss of endothelial glycocalyx during accute hyperglicaemia [3].

If you want to know more about it read the articles below:

[1] Dunne, M. (2002). "Baterial adhesion: Seen any good biofilms lately?". Clinical microbiology reviews, 15(2), pp. 155-166.

[2] Rabelink and Zeeuw (2015). "The glycocalyx - linking albuminuria with renal and cardiovascular disease". Nature Reviews Nephrology, advanced online publication.

[3] Nieuwdorp et al., (2006). "Loss of endothelial glycocalyx during acute hyperglicemia coincides with endothelialdysfunction  and coagulation  activation in vivo". Diabetes, 55(2), pp. 480-486.

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