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dc.contributorDepartment of Applied Biology and Chemical Technologyen_US
dc.creatorYu, Men_US
dc.creatorChua, SLen_US
dc.publisherJohn Wiley & Sonsen_US
dc.rights© 2019 Wiley Periodicals, Incen US
dc.rightsThis is the peer reviewed version of the following article: Yu, M, Lin Chua, S. Demolishing the great wall of biofilms in Gram-negative bacteria: To disrupt or disperse? Med Res Rev. 2020; 40: 1103–1116, which has been published in final form at This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions. This article may not be enhanced, enriched or otherwise transformed into a derivative work, without express permission from Wiley or by statutory rights under applicable legislation. Copyright notices must not be removed, obscured or modified. The article must be linked to Wiley’s version of record on Wiley Online Library and any embedding, framing or otherwise making available the article or pages thereof by third parties from platforms, services and websites other than Wiley Online Library must be prohibited.en US
dc.subjectAntimicrobial treatmenten_US
dc.subjectChronic infectionsen_US
dc.titleDemolishing the great wall of biofilms in Gram‐negative bacteria : to disrupt or disperse?en_US
dc.typeJournal/Magazine Articleen_US
dcterms.abstractBacterial infections lead to high morbidity and mortality globally. While current therapies against bacteria often employ antibiotics, most bacterial pathogens can form biofilms and prevent effective treatment of infections. Biofilm cells can aggregate and encased themselves in a self‐secreted protective exopolymeric matrix, to reduce the penetration by antibiotics. Biofilm formation is mediated by c‐di‐GMP signaling, the ubiquitous secondary messenger in bacteria. Synthesis of c‐di‐GMP by diguanylate cyclases leads to biofilm formation via the loss of motility, increased surface attachment, and production of biofilm matrix, whereas c‐di‐GMP degradation by phosphodiesterases causes biofilm dispersal to new sites via increased bacterial motility and matrix breakdown. The highly variable nature of biofilm development and antimicrobial tolerance imposes tremendous challenges in conventional antimicrobial therapies, indicating an imperative need to develop anti‐biofilm drugs against biofilm infections. In this review, we focus on two main emergent approaches—active dispersal and disruption. While both approaches aim to demolish biofilms, we will discuss their fundamental differences and associated methods. Active dispersal of biofilms involves signaling the bacterial cells to leave the biofilm, where resident cells ditch their sessile lifestyle, gain motility and self‐degrade their matrix. Biofilm disruption leads to direct matrix degradation that forcibly releases embedded biofilm cells. Without the protection of biofilm matrix, released bacterial cells are highly exposed to antimicrobials, leading to their eradication in biofilm infections. Understanding the advantages and disadvantages of both approaches will allow optimized utility with antimicrobials in clinical settings.en_US
dcterms.accessRightsopen accessen_US
dcterms.bibliographicCitationMedicinal research reviews, May 2020, v. 40, no. 3, p. 1103-1116en_US
dcterms.isPartOfMedicinal research reviewsen_US
dc.description.validate202010 bcrcen_US
dc.description.oaAccepted Manuscripten_US
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