Advanced strategies for combating bacterial biofilms

Abstract

Biofilms are communities of microorganisms that are formed on and attached to living or nonliving surfaces and are surrounded by an extracellular polymeric material. Biofilm formation enjoys several advantages over the pathogens in the colonization process of medical devices and patients' organs. Unlike planktonic cells, biofilms have high intrinsic resistance to antibiotics and sanitizers, and overcoming them is a significant problematic challenge in the medical and food industries. There are no approved treatments to specifically target biofilms. Thus, it is required to study and present innovative and effective methods to combat a bacterial biofilm. In this review, several strategies have been discussed for combating bacterial biofilms to improve healthcare, food safety, and industrial process.

Interactions of Gold and Silver Nanoparticles with Bacterial Biofilms: Molecular Interactions behind Inhibition and Resistance

“…Comprehensive analysis of the multicomponent nature of the biofilm has chalked out few excellent targets for combating microbial infections and infectious diseases [ 1 , 8 , 9 ]. The biofilm inhibition approaches can be categorized into four classes: (i) targeting bacterial adhesion and EPS components, (ii) targeting biofilm metabolism, (iii) facilitating biofilm dispersal and (iv) targeting dormant cells [ 7 , 8 , 9 , 10 ]. The early stages of biofilm formation (i.e., bacterial adhesion and EPS synthesis) can be targeted using molecules such as bacterial adhesion inhibitors (mannoside derivatives), cyclic-di-GMP pathway targeting molecules (e.g., cephalosporin-3′-diazeniumdiolate) and inhibitors of lipopolysaccharide (LPS) synthesis enzymes (e.g., LpxC inhibitors) [ 7 , 8 , 9 , 10 ].…”

“…The biofilm inhibition approaches can be categorized into four classes: (i) targeting bacterial adhesion and EPS components, (ii) targeting biofilm metabolism, (iii) facilitating biofilm dispersal and (iv) targeting dormant cells [ 7 , 8 , 9 , 10 ]. The early stages of biofilm formation (i.e., bacterial adhesion and EPS synthesis) can be targeted using molecules such as bacterial adhesion inhibitors (mannoside derivatives), cyclic-di-GMP pathway targeting molecules (e.g., cephalosporin-3′-diazeniumdiolate) and inhibitors of lipopolysaccharide (LPS) synthesis enzymes (e.g., LpxC inhibitors) [ 7 , 8 , 9 , 10 ]. Early biofilms and mature biofilms can be eradicated using structural protein inhibitors (e.g., ring-fused 2-pyridones), eDNA-targeting molecules (e.g., alginate derivatives), QS inhibitor peptides (e.g., AIP-I or RIP), EPS-degrading enzymes (e.g., glucanohydrolases or dispersin) and monoclonal antibodies (e.g., Ebp A) [ 7 , 8 , 9 , 10 ].…”

“…The early stages of biofilm formation (i.e., bacterial adhesion and EPS synthesis) can be targeted using molecules such as bacterial adhesion inhibitors (mannoside derivatives), cyclic-di-GMP pathway targeting molecules (e.g., cephalosporin-3′-diazeniumdiolate) and inhibitors of lipopolysaccharide (LPS) synthesis enzymes (e.g., LpxC inhibitors) [ 7 , 8 , 9 , 10 ]. Early biofilms and mature biofilms can be eradicated using structural protein inhibitors (e.g., ring-fused 2-pyridones), eDNA-targeting molecules (e.g., alginate derivatives), QS inhibitor peptides (e.g., AIP-I or RIP), EPS-degrading enzymes (e.g., glucanohydrolases or dispersin) and monoclonal antibodies (e.g., Ebp A) [ 7 , 8 , 9 , 10 ]. The metabolism of the biofilms can be disrupted using exogenously administered amino acids (e.g., L-arginine or L-methionine) or metals (e.g., gallium), which hamper particular metabolic pathways, promote biofilm disassembly and make them vulnerable to classical antibiotics [ 7 , 8 , 9 , 10 ].…”

<p>The Battle of Probiotics and Their Derivatives Against Biofilms</p>

“…1 Hardly are biofilms detectable with routine diagnostic tests; therefore, the management of their infections are challenging in the clinic. 2 Methicillinresistant Staphylococcus aureus (MRSA), Streptococcus mutans, Pseudomonas aeruginosa, S. epidermidis and Gardnerella vaginalis are the most common biofilm formers in the clinic. 3 Different strategies like new generations of antibiotics and the inhibition of biofilm formation by quorum sensing (QS) inhibitors have been developed.…”

Vesicle-associatedPseudomonas aeruginosaleucine aminopeptidase modulates bacterial biofilms grown on host cellular substrates

“…Longitudinal studies that follow the progression of P. aeruginosa strains from early colonization through chronic infection have shown that the bacteria quickly evolve and adapt to the conditions found in the CF lung, and that many of the genetic changes seen in chronic P. aeruginosa strains function to decrease overall bacterial pathogenicity [32][33][34] . For example, mucA mutations, which downregulate the expression of virulence-associated type III secretion systems, are frequently observed 35,36 . Additionally, researchers have found mutations that decrease quorum sensing and, notably for this discussion, biofilm formation 32,33 .…”