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Category: Environmental Microbiology
Dispersal from Microbial Biofilms, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555817466/9781555817459_Chap17-1.gif /docserver/preview/fulltext/10.1128/9781555817466/9781555817459_Chap17-2.gifAbstract:
For all organisms the ability to spread and colonize new habitats is crucial to ensure species continuity and prevent extinction ( 1 ). In sessile organisms this constraint has led to the evolution of a motile, dispersal phase in their life cycle, which in plants and corals involves the release of differentiated and often phenotypically diverse seeds or propagules. Similarly, sessile microbial biofilms have developed mechanisms to release differentiated, highly motile dispersal cells into the bulk liquid.
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Microscopic images of biofilm microcolonies during seeding dispersal. (A-B) Motile cells appear in mature biofilm microcolonies. (A) Single frame of a mature microcolony. (B) Picture showing the average of 30 frames captured over a 1-second period. The highly motile cells “average” out and appear blurred in the center of the microcolony, demonstrating the extent of the motile region (white arrow in panels A and B). The sessile “wall” region is indicated by the black arrows in panel A (taken from reference 26 , with permission from the publisher). (C) Live/dead staining of a 7-day-old biofilm reveals patterns of cell death inside biofilm structures that occur simultaneously with biofilm dispersal, as indicated by the formation of hollow biofilm structures. Live cells are green and dead cells are red (adapted from reference 56 , copyright © American Society for Microbiology). (D) XZ cross-view of the biofilm in panel C (XY view) at the location indicated by the white line.
Effectors of biofilm dispersal. Bacteria within the center of microcolonies induce a number of mechanisms to degrade and solubilize the biofilm EPS matrix and extracellular appendages such as fimbriae that immobilize cells. When the interior of the microcolony becomes fluid, cells begin to show signs of motility, and a breach is made in the microcolony wall through which dispersal cells are released.
Physiological traits of planktonic, biofilm, and dispersal cells. Symbols are defined in Figure 2 .
A range of strategies targeting dispersal have been developed to control biofilms and biofilm-related infections. (a) BdcA protein with enhanced c-di-GMP binding ( 124 ). (b) Oroidin and synthetic derivatives that were identified as potent dispersal inducers after screening chemical libraries ( 125 ). (c) Diffusible fatty acid signal cis-2-decenoic acid ( 23 ). (d) Furanone 30, a synthetic QS inhibitor derived from natural furanone compounds isolated from the red alga Delisea pulchra ( 131 ). (e) Fimbrolide-nitroester with dual action QS inhibition and NO release ( 134 ). (f) β-lactam-NO prodrugs for the targeted delivery of NO to infectious biofilms ( 132 ). (g) Controlled delivery of NO using nanoparticles ( 135 ). (h) Catalytic generation of NO from endogenous nitrite sources to disperse and prevent biofilm for long-term applications ( 138 ).