Biofilm Dispersal: Mechanisms, Clinical Implications, and Potential Therapeutic Uses

Abstract

Like all sessile organisms, surface-attached communities of bacteria known as biofilms must release and disperse cells into the environment to colonize new sites. For many pathogenic bacteria, biofilm dispersal plays an important role in the transmission of bacteria from environmental reservoirs to human hosts, in horizontal and vertical cross-host transmission, and in the exacerbation and spread of infection within a host. The molecular mechanisms of bacterial biofilm dispersal are only beginning to be elucidated. Biofilm dispersal is a promising area of research that may lead to the development of novel agents that inhibit biofilm formation or promote biofilm cell detachment. Such agents may be useful for the prevention and treatment of biofilms in a variety of industrial and clinical settings. This review describes the current status of research on biofilm dispersal, with an emphasis on studies aimed to characterize dispersal mechanisms, and to identify environmental cues and inter-and intracellular signals that regulate the dispersal process. The clinical implications of biofilm dispersal and the potential therapeutic applications of some of the most recent findings will also be discussed.

Dispersed cells represent a distinct stage in the transition from bacterial biofilm to planktonic lifestyles

“…1). Hence, the dispersed cells were, until now, thought to be similar to planktonic cells and assumed to be easily eradicated by the host immune system and antimicrobials 6 .…”

“…It is estimated that biofilms are responsible for 65-80% of the infections occurring in the human body 5 , which, due to their persistence and chronic nature, place a massive burden on healthcare systems worldwide. Through dispersal processes, biofilms can spark new infections within the host and result in the transmission of bacteria between different hosts 4,6 . One medically relevant biofilm-forming bacterium is the opportunistic pathogen Pseudomonas aeruginosa, which is primarily known for its involvement in cystic fibrosis 7 , catheter-related infections 8 , and eye 9 and chronic wound infections 10 .…”

IS5 inserts upstream of the master motility operon flhDC in a quasi-Lamarckian way

“…In the presence of glass wool, planktonic cells were collected from the culture, and biofilm cells were collected from the glass wool by sonicating. Motility results indicated that a small proportion of biofilm cells (as early as 8 h) migrated much faster than the rest of the non-motile cells, which Figure 3a); however, these motile cells are probably derived from the biofilms as no highly motile cells arise in shaking flasks without biofilms, and cells frequently detach from biofilms (Kaplan, 2010). After 15 h, 24 h and 39 h of incubation, the proportion of highly motile cells increased for both biofilm and planktonic cells in contact with biofilms.…”

“…Flagella are important for initial attachment in biofilms (Pratt and Kolter, 1998), for the mature structure , and for the dispersal of biofilms (Kaplan, 2010). Here, we tested whether IS5 is inserted upstream of flhD þ during biofilm development by screening biofilm cells for increases in motility.…”

Extracellular matrix structure governs invasion resistance in bacterial biofilms

“…If nutrient sources persist, biofilms can grow into structures many orders of magnitude larger than individual cells. By contrast, if resources become depleted, bacteria can disperse back into the planktonic phase, presumably to encounter new locations with superior resource availability (Kaplan, 2010;Landini et al, 2010;McDougald et al, 2012). The ability of planktonic bacteria to adhere to naked surfaces and initiate biofilm formation has been studied extensively (Beachey, 1981;Palmer et al, 2007).…”