Development of a rapid startup technology applicable to autotrophic nitrogen removal

氨氧化细菌(AOB)和厌氧氨氧化细菌(Anammox)由于其自养性质，生长速度较慢，这一直是工程上的一个挑战。为了缩短完全自养脱氮工艺的启动时间，对细菌载体表面进行了化学修饰，以吸引细菌附着和生物膜形成。由于已有报道表明这些细菌生物膜的形成可能是通过群体感应(QS)机制作为细胞间的通讯来介导的，因此本研究的另一个目的是阐明AOB和厌氧氨氧化细菌的生物膜形成机制。采用辐射诱导接枝聚合(RIGP)方法，将甲基丙烯酸缩水甘油酯(GMA)化学接枝到由聚乙烯制成的无纺布上。GMA的环氧基被转化为二乙胺(DEA片层)，形成对细菌黏附具有吸引力的带正电荷的表面。DEA膜能快速固定AOB，其固定率是纯无纺布膜的104倍。AOB培养9d后，DEA膜的氨氧化速率比纯膜高4.4倍。DEA膜强化了厌氧氨氧化细菌污泥的固定化，其厌氧氨氧化速率是纯无纺布膜的2.4倍，制备了一种酶固定化膜来阻断细菌细胞之间的细胞间通讯，从而触发生物膜的形成。将能够降解QS介导的信号转导化合物N-酰基-L-高丝氨酸内酯(AHLS)的酰基酶I固定在DEA薄片上。与非织造布相比，AOB生物膜不那么结实，也更稀疏。这表明，没有细胞间通讯的AOB生物膜在纸上被抑制，因为生物膜中的AHL被分解。另一方面，在厌氧氨氧化生物膜方面没有观察到这一趋势。另一种机制参与了生物膜的形成。

Ammonia-oxidizing bacteria (AOB) and anaerobic ammonium-oxidizing (anammox) bacteria have slow growth rates due to their autotrophic nature, which is always an engineering challenge. In order to shorten the startup time of a process for completely autotrophic nitrogen removal, surface of a bacterial carrier was chemically modified to attract bacterial adhesion and biofilm formation. Since it has been reported that these bacterial biofilm formations are potentially mediated by quorum sensing (QS) mechanism as cell-cell communication, another objective of the study was to elucidate biofilm formation mechanisms of AOB and anammox bacteria. Radiation-induced graft polymerization (RIGP) was applied to chemically graft glycidyl methacrylate (GMA) on a non-woven sheet made of polyethylene. The epoxy-group of GMA was converted into diethylamine (DEA sheet) to form a positively-charged surface attractive to bacterial adhesion. The DEA sheet immobilized AOB rapidly, the rate of which was 104-fold as high as a pristine non-woven sheet. After 9 day of AOB incubation, ammonia oxidation rate of DEA sheet was higher than that of the pristine sheet by a factor of 4.4. The DEA sheet enhanced immobilization of anammox bacterial sludge, resulting in 2.4 times higher anammox rate than that on a pristine non-woven sheet.An enzyme-immobilized sheet was fabricated to interrupt cell-cell communication among bacterial cells, which is a trigger to form biofilm. Acylase I, capable of degradingQS-mediated signaling compounds, i.e. N-acyl-L-homoserine lactones (AHLs), was immobilized onto a DEA sheet. AOB biofilm on this sheet was less robust and rather more sparse than that on a pristine non-woven sheet. This suggests that AOB biofilm without cell-cell communication was suppressed on the sheet because of breaking down AHLs in the biofilm. On the other hand, this trend was not observed regarding anammox biofilm. Another mechanism was involved to form the biofilm.