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Suppressing Bacterial Biofilms through Molecular Communications

By 26th September 2018 No Comments

Antimicrobial resistance has become a global concern in recent years, and new techniques are continually being sought to treat bacterial infections without enhancing its resistance capabilities. A common approach is to quench the bacterial signalling molecules responsible for the formation of a structure that protects the bacteria from external attacks. A bacterial population living inside of this protective structure is called biofilm, and it can grow around implantable devices and usually leads to infection. A general illustration of the proposed model. The biofilm formation initiates when the bacteria find a suitable surface to attach. However, as a second bacteria population also arrives at the same location and start to produce the pulse-based jamming signal the biofilm does not form.

Researchers at the TSSG, using proteomic results from wet lab experiments*, were able to model the signalling pathways associated with the formation of biofilms as communication channels.  Based on these channel models, the researchers identified suitable suppression signals that can be used to disrupt the communication process of the biofilms. This suppression process is akin to jamming techniques used as a security attack in wireless communication networks. Fig. 1 illustrates the process of jamming the signals from engineered bacteria (JN) that will disrupt the communication process of the bacteria (TN and RN) forming the biofilm.

Fig1

 

 

 

 

 

 

Figure 1. A general illustration of the proposed model. The biofilm formation initiates when the bacteria find a suitable surface to attach. However, a second bacterial population in the same location produces the pulse-based jamming signals to suppress and jam the communication process for forming the biofilm.  

In this work, two different bacterial populations were considered. One was the biofilm-forming bacteria (Staphylococcus aureus – S. aureus) while the other was engineered to produce the molecular pulse-based jamming signal (Streptomyces sp.). As identified by studying the wet lab experiment results, the biofilm formation is a cascaded multistep process which involves three main communications channels: defence, cellular stress and energy regulation. Therefore, the molecular pulse-based jamming signal when received by the S. aureus, will disrupt the production of specific proteins for each communications channels, and, consequently suppress the biofilm formation.

The biofilm suppression process was analysed by varying different parameters that include the distance between the bacterial populations, molecular pulse-based jamming signal power and its transmission delay. Using this analysis, the researchers could measure the path loss for the molecular pulse-based jamming signals used for the bacterial biofilm suppression. Fig. 2 demonstrates an example result from the study that shows the channel attenuation increases proportionally to the number of engineered bacteria and it also increases when there is no delay in the transmission of the molecular pulse-based jamming signal.

Fig2

 

Figure 2. The channel attenuation caused by low and high power molecular pulse-based jamming signals when they suffer from different transmission delays.

The research could be used to prevent and curb the increasing number of antibiotic-resistant bacteria, and also defines the fundamental parameters required to design a bacteria-based molecular communications system that is capable of interfering with the natural communication process.

*This research was conducted in collaboration with Department of Genetics, Kasetsart University, Thailand.

Publication Title: Molecular Communications Pulse-based Jamming Model for Bacterial Biofilm Suppression

Authors: Daniel P. Martins, Kantinan Leetanasaksakul, Michael Taynnan Barros, Arinthip Thamchaipenet, William Donnely, Sasitharan Balasubramaniam

Journal: IEEE Transactions on Nanobioscience (to appear, 2018)

Link: https://ieeexplore.ieee.org/document/8468188/