Difference between revisions of "Team:WPI-Worcester/Background"

Background

Biofilms

Biofilms are a way in which single-celled organisms can act in a multicellular manner through cooperation. They are strongly resistant to antimicrobials (Donlan and Costerton 2002), which means that combating them is an important step in the fight against healthcare-associated infections, which have many times been shown to be associated with medical devices or surgical sites that are colonized by biofilms (Abdallah et al. 2014), which are thought to be causative (Akers et al. 2015). Biofilms are also the primary source—and a persistent one—of food product contamination (Abdallah et al. 2014).

Biofilms are largely made up of an extracellular matrix that is produced by the organisms. The matrix composes 90% of the biomass in a given biofilm, and is made up of extracellular polymeric substances, carbohydrate-binding proteins, pili, flagella, adhesive fibers, and extracellular DNA (Kostakioti et al. 2013).

Biofilm formation occurs in steps. The first step is introduction of bacteria to a surface, which is followed by the second step, adhesion. Motile bacteria have an advantage in this step; flagella allow bacteria to overcome forces that might otherwise prevent attachment (Kostakioti et al. 2013). Other extracellular appendages, and adhesins secreted by the bacteria, affect adhesion as well. However, initial adhesion is reversible based on repulsive or hydrodynamic forces, or the availability of nutrients. If the bacteria are capable of sticking despite those forces, they will become irreversibly attached. Irreversible attachment is facilitated by a variety of factors, including type 1 and type IV pili, curli fibers, and Antigen 43 (Kostakioti et al. 2013). Surface contact results in the up-regulation of genes that will make the bacteria become sessile—that is, anchored.

Following attachment, dispersal can occur. Dispersal can be passive (as a result of shear forces) or active, as in a bacterial response to detected environmental factors, such as oxygen levels or nutrient availability. Occasionally dispersal can occur in other ways; for example, in B. subtilis, fluctuations in certain amino acid levels over the course of the cell cycle can result in dispersal, and it’s been suggested that similar mechanisms could exist in other bacteria (Kostakioti et al. 2013).

In 2014, Heisig et al. found that an antifreeze glycoprotein from ticks, IAFGP, and a peptide derived from that protein, could inhibit the formation of S. aureus biofilms in a variety of in vitro and in vivo scenarios. Figure 1C from the study, below, shows the results of an in vitro biofilm inhibition assay, performed by staining with Safranin.

The current research suggests that the anti-virulent properties of IAFGP are based on structural elements of the protein that allow it to bind to microbes and disrupt biofilm formation (Heisig et al. 2014), however, very little is known about this, and only one study has been completed. More research is needed to find out whether other antifreeze proteins exhibit the same effect.