Time to leave: biofilm dispersal and implications for the host

A mature biofilm community can persist for extended periods of time, owing to the ECM and the different subpopulations that arise within it. However, as the biofilm matures, bacteria from within the community can disperse from the biomass into the surrounding environment (Fig. 3.2(f)). Dispersed bacteria can then seed secondary-site infection in biofilm- or planktonic states.

The signal(s) to leave: cues lending to dissemination from the bio film

Perhaps the least understood stage in the biofilm-formation pathway is dispersal from the biomass. To date, dispersal mechanisms have been the most well studied in P. aeruginosa, and several different mechanisms of dissemination have been uncovered (Hall-Stoodley and Stoodley, 2005; Kaplan, 2010; Kostakioti et al., 2013).

Perhaps the biggest cue for dissemination from the biofilm is an increase in cell density that reaches a threshold size, becoming a limiting factor to biofilm growth (Parsek and Greenberg, 2005). Quorum sensing plays a major role in mediating population density-dependent changes and has thus been implicated in biofilm dispersal (Parsek and Greenberg, 2005). In S. aureus, autoinducing peptides (as well as glucose starvation) signal dispersal from the biofilm through activation of the agr quorum sensing system and mediation of extracellular serine protease activity (Boles and Horswill, 2008). Increased expression of D-amino acids within biofilms can also serve as signals for dispersal, even though these studies have been controversial owing to a mutation within a particular strain used in these studies (Cava et al., 2010; Kolodkin-Gal et al., 2010).

Nutrient availability can play a dual role in controlling dispersal. In some examples, nutrient-limiting conditions induce dispersal from the biomass allowing bacteria to depart the community in search of new nutrient sources. Conversely, an increase in nutrient availability can also induce dissemination from the biomass (Sauer et al., 2004). This could be the case where nutrient-limiting conditions originally initiated biofilm formation, and upon an increase in nutrient availability in the surrounding environment, bacteria can return to life in a planktonic state.

Atmospheric cues can also lead to dissemination from the biofilm. In P. aeruginosa biofilms, dispersal can be signaled through nitric oxide (NO) (Barraud et al., 2006, 2015; Kirov et al., 2007; Romeo, 2006). As oxygen availability decreases, bacteria switch to anaerobic forms of respiration, one by-product of which is the generation of NO. In Section 3.2.4, we highlighted how the shift from planktonic bacteria to a biofilm state is largely governed by an increase in intracellular cyclic-di-GMP levels. Data suggests that an increase in NO levels in P. aeruginosa and other bacterial species (Plate and Marietta, 2012) can signal dispersal through increasing phosphodiesterase activity that reduces intracellular c-di-GMP levels (Barraud et al., 2009). This decrease in c-di-GMP would reverse the planktonic to sessile signaling that initiated biofilm formation, thereby allowing bacteria to become motile once again and leave the community. NO has also been implicated in the dispersal mechanism of Neisseria gonorrheae (Falsetta et al., 2010). Another interesting mechanism by which P. aeruginosa biofilms have been proposed to disperse is through the production of rhamnolipids that act as a biosurfactant to disrupt interactions of bacteria with the surface (Boles et al., 2005; Pamp and Tolker-Nielsen, 2007).

Dispersal from the original site of biofilm-associated infection can exacerbate the initial infection or can result in secondary-site infections that further complicate treatment and bring great risk to the host.

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