An Overview of Biofilm Formation-Combating Strategies and Mechanisms of Action of Antibiofilm Agents

Abstract

Biofilm formation on surfaces via microbial colonization causes infections and has become a major health issue globally. The biofilm lifestyle provides resistance to environmental stresses and antimicrobial therapies. Biofilms can cause several chronic conditions, and effective treatment has become a challenge due to increased antimicrobial resistance. Antibiotics available for treating biofilm-associated infections are generally not very effective and require high doses that may cause toxicity in the host. Therefore, it is essential to study and develop efficient anti-biofilm strategies that can significantly reduce the rate of biofilm-associated healthcare problems. In this context, some effective combating strategies with potential anti-biofilm agents, including plant extracts, peptides, enzymes, lantibiotics, chelating agents, biosurfactants, polysaccharides, organic, inorganic, and metal nanoparticles, etc., have been reviewed to overcome biofilm-associated healthcare problems. From their extensive literature survey, it can be concluded that these molecules with considerable structural alterations might be applied to the treatment of biofilm-associated infections, by evaluating their significant delivery to the target site of the host. To design effective anti-biofilm molecules, it must be assured that the minimum inhibitory concentrations of these anti-biofilm compounds can eradicate biofilm-associated infections without causing toxic effects at a significant rate.

Keywords: antibiofilm agents; antibiotic resistance; antibodies; biofilms; combating strategies; nanomaterials; natural products.

Figure 1

Phases of biofilm formation.

Figure 2

Chemical structures of some anti-biofilm compounds that inhibit AHL-mediated QS. (a) AHL, (b) triazole dihydro furanone, (c) synthetic halogenated furanone, (d) EGCG, (e) ellagic acid.

Figure 3

QS in Gram-negative bacteria; some bacteria can secrete AHL that enters neighboring cells and induce the QS-mediated formation of virulence factors and biofilm development.

Figure 4

Chemical structures of some anti-biofilm compounds that inhibit AHL-mediated QS. (a) quercetin, (b) curcumin, (c) allicin, (d) ajoene, (e) baicalin hydrate.

Figure 5

Mechanism of action of AMPs on the membrane system of Gram-negative and Gram-positive bacteria. In Gram-negative bacteria, the AMP outreach the cytoplasmic membrane via permeabilizing the outer membrane, while in Gram-positive bacteria, the AMP directly disperses through nano ranged pores of the peptidoglycan layer. After binding to the inner membrane, APMs can create three types of pores (barrel-stave pore, toroidal pore, or carpet model). Adapted from Jianguo et al. 2017, [131].

Figure 6

Anti-biofilm activity of surface engineered NPs with different antimicrobial effects (adapted from Lee et al. [244]).

Figure 7

Chemical structures of the anti-biofilm compounds with unknown mode of action; (a) fisetin, (b) esculetin, (c) octenidine hydrochloride.