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Review
. 2021 Feb;47(1):57-78.
doi: 10.1080/1040841X.2020.1842325. Epub 2020 Dec 28.

Ways to control harmful biofilms: prevention, inhibition, and eradication

Wen Yin  1 , Siyang Xu  1 , Yiting Wang  1 , Yuling Zhang  1 , Shan-Ho Chou  1 , Michael Y Galperin  2 , Jin He  1
Affiliations
Review

Ways to control harmful biofilms: prevention, inhibition, and eradication

Wen Yin et al. Crit Rev Microbiol. 2021 Feb.

Abstract

Biofilms are complex microbial architectures that encase microbial cells in a matrix comprising self-produced extracellular polymeric substances. Microorganisms living in biofilms are much more resistant to hostile environments than their planktonic counterparts and exhibit enhanced resistance against the microbicides. From the human perspective, biofilms can be classified into beneficial, neutral, and harmful. Harmful biofilms impact food safety, cause plant and animal diseases, and threaten medical fields, making it urgent to develop effective and robust strategies to control harmful biofilms. In this review, we discuss various strategies to control biofilm formation on infected tissues, implants, and medical devices. We classify the current strategies into three main categories: (i) changing the properties of susceptible surfaces to prevent biofilm formation; (ii) regulating signalling pathways to inhibit biofilm formation; (iii) applying external forces to eradicate the biofilm. We hope this review would motivate the development of innovative and effective strategies for controlling harmful biofilms.

Keywords: Harmful biofilm; biofilm control; infected tissue; medical device; tissue implant.

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Conflict of interest statement

Conflicts of Interest

The authors declare no conflict of interest.

Figures

Figure 1.
Figure 1.. Schematic diagram of biofilm effects.
On one hand, biofilms play beneficial roles in wastewater treatment, biodegradation and bioremediation, and geochemical cycles of various elements. On the other hand, biofilms affect human life and health, contaminating medical implants and devices and causing a variety of infections.
Figure 2.
Figure 2.. Strategies for controlling harmful biofilms.
(A) Material surfaces can be treated through thermal cycling and UV irradiation. (B) Surfaces can be coated by 2-methacryloyloxyethyl phosphorylcholine (MPC)-polymers, trimethylsilane (TMS)/O2, and antimicrobial peptides. (C) Biofilm formation can be inhibited by chemical agents that influence quorum sensing (QS), c-di-GMP, c-di-AMP, and (p)ppGpp related pathways. (D) External force, including biochemical substances and ultrasound, can also be applied to eradicate mature biofilms.
Figure 3.
Figure 3.. Cyclic di-GMP regulates biofilm formation by inhibiting bacterial motility and increasing EPS production.
(A) Binding of c-di-GMP to the bacterial flagellar brake protein YcgR inhibits the rotation of the flagellar motor, reduces cell motility, and promotes bacterial attachment to the solid surface. (B) Binding of c-di-GMP to MshE promotes the assembly of mannose-sensitive haemagglutinin pilus and helps the bacterial attachment to the solid surface. (C-E) C-di-GMP promotes the synthesis of bacterial EPS and solidifies biofilm formation: (C) When intracellular c-di-GMP concentration reaches a certain threshold, the inhibition of YdaM and MlrA proteins by YciR is relieved. YdaM can activate MlrA to interact with the central curli regulator CsgD, which induces the transcription of curli genes and facilitates curli formation; (D) Bacterial cellulose synthetase catalytic subunit BcsA is anchored on the inner membrane. When c-di-GMP binds to BcsA, its glycosyltransferase domain is activated to assemble the nascent polysaccharide with the help of BcsB/BcsC/BcsZ complex to form extracellular cellulose; (E) The PgaABCD complex promotes formation of the exopolysaccharide poly-GlcNAc. PgaC and PgaD interact with the help of c-di-GMP to form the PgaCD glycosyltransferase complex, which is used for the polymerization and extension of poly-GlcNAc. PgaA and PgaB are responsible for the transport of poly-GlcNAc outside the cell. IM, inner or plasma membrane; PG, peptidoglycan; OM, outer membrane.
Figure 4.
Figure 4.. Applying external pressure to eradicate mature biofilm.
(A) Ultrasound directly eradicates biofilm from the solid surface. (B) Phage lysins effectively kill bacteria in the biofilm through cleaving bacterial peptidoglycan. (C) Degradative enzymes eradicate biofilm by degrading the polysaccharide and eDNA in the EPS matrix. (D) Microbial metabolites disrupt bacterial cell membrane or regulate bacterial physiological activity to eradicate the biofilm.
Figure 5.
Figure 5.. Applying phage lysins to eradicate mature biofilm.
Phage lysins such as LysGH15, CF-301, LysH5, and P128 can cleave the peptidoglycan of microbial cell walls enzymatically and therefore promote biofilm dispersal.
Figure 6.
Figure 6.. Applying phage lysins to eradicate mature biofilm.
Phage lysins such as LysGH15 (Zhang et al. 2018), CF-301 (Schuch et al. 2017), LysH5 (Gutierrez et al. 2014), and P128 (Poonacha et al. 2017) can enzymatically cleave the peptidoglycan of cell walls to kill staphylococci.
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