A new filamentous bulking control strategy: The role of N-acyl homoserine lactone (AHL)-mediated quorum sensing in filamentous bacteria proliferation within activated sludge

Abstract

The microcosmic mechanisms underlying filamentous bulking are still unclear. Quorum sensing (QS) is an important mechanism by which bacteria control self-reproduction and growth in response to changes in population density. The potential role of QS in filamentous bulking and the feasibility of using a Quorum quenching (QQ) strategy to inhibit filamentous bulking were investigated in this study. The results indicated that the rate of increase in the population density and the abundance of filamentous bacteria in the serious filamentous bulking stage (250 mL/g < SVI) was 1.46 and 2.76 times greater, respectively, than that of the limited filamentous bulking stage (150 mL/g < SVI < 250 mL/g). The proliferation of filamentous bacteria was clearly population density-dependent. The concentration of C6-HSL increased from 31.39 ± 3.52 ng/g VSS to 125.29 ± 6.70 ng/g VSS with an increase in the abundance of filamentous bacteria. Filamentous bulking could be promoted by exogenous N-acyl homoserines (AHLs), especially C6-HSL. The hdtS gene related to the synthesis of AHLs and the lasR and cciR genes related to receptors showed significantly increased expressions during filamentous bulking. SDHA, ND1, and CDK2 genes related to proliferation showed significantly increased expression during filamentous bulking. The QS-AHL system was triggered during filamentous bulking, which promoted the proliferation of filamentous bacteria. As expected, filamentous bulking was significantly inhibited by the addition of vanillin, a quorum sensing inhibitor. Therefore, QQ is a potential strategy for the prevention and control of filamentous bulking. This study provides new information regarding the microcosmic mechanisms of filamentous bulking.