目前甲砜霉素的生物降解机理尚未清楚，阐明该机理对加强环境中甲砜霉素的生物去除具有重要意义。本研究利用三种氯霉素类抗生素建立高浓度好氧活性污泥驯化体系，富集甲砜霉素高效降解菌群，通过多组学（包括宏基因组、宏转录组和非靶向代谢组学）数据整合分析了菌群微生物对抗生素的去除特征、混合菌群的群落组成、基因组功能和代谢路径，并揭示了甲砜霉素的生物降解机理。 好氧活性污泥经过驯化可以有效降解甲砜霉素和氯霉素，无法降解氟苯尼考。16S扩增子测序和宏基因组测序揭示了微生物群落组成及其演替，发现随着驯化时间的增长和抗生素浓度的提高，微生物多样性显著下降。变形菌门是所有微生物群落中的优势菌门，其中念珠菌竞争杆菌则是优势菌属。群落的动态演替主要受抗生素浓度变化的影响。通过降解产物分析，揭示了三条甲砜霉素生物转化途径，分别是甲砜霉素C3-OH的乙酰化生成Ac-TAP、C3-OH氧化为羧基生成O-TAP、C3-OH被氧化成醛和C1-OH脱氢生成dD-TAP。通过多组学数据整合分析预测了多个参与甲砜霉素生物转化的关键基因。其中噬氢菌携带的GDH 氧化还原酶（基因名capO2）是负责甲砜霉素C3和C1羟基氧化的关键酶。热单胞菌属携带的乙酰转移酶基因的表达在甲砜霉素快速降解过程中显著增加，这与甲砜霉素乙酰化产物的生成规律相一致。因此，热单胞菌通过C3-OH乙酰化的方式使甲砜霉素失活。 通过非靶向代谢组学方法揭示了胞内差异代谢物和胞外差异代谢物，通过KEGG通路富集分析发现甲砜霉素主要影响了菌群类固醇生物合成途径、亚油酸代谢途径、二级胆汁酸生物合成和不饱和脂肪酸的生物合成。

At present, the biodegradation mechanism of thiamphenicol is not clear, and it is of great significance to clarify the mechanism for enhancing the biological removal of thiamphenicol from the environment. In this study, three chloramphenicol antibiotics were used to establish a high-concentration aerobic activated sludge acclimation system, and the efficient degrading bacteria of thiamphenicol were enriched. Multi-omics （including metagenomics, meta-transcriptomics and non-targeted metabolomics） were integrated to analyze the antibiotic removal characteristics of microbial consortia, community composition, genomic function and metabolic pathway. The biodegradation mechanism of thiamphenicol was also revealed.Aerobic activated sludge can effectively degrade thiamphenicol and chloramphenicol after acclimation, but not florfenicol. 16S amplicon sequencing and metagenomic sequencing revealed microbial community compositions and succession patterns. A significant decline in microbial diversity with increasing domestication time and antibiotic concentration was observed. Proteobacteria is the dominant phylum in all microbial communities, among which Candidatus_Competibacter is the dominant genus. The dynamic succession of the community is mainly affected by the change of antibiotic concentration.Through the analysis of degradation products, thiamphenicol was found to be catabolized in three pathways including the acetylation of thiamphenicol C3-OH producing Ac-TAP, the oxidation of C3-OH to carboxyl group producing O-TAP, the oxidation of C3-OH to aldehyde, and the dehydrogenation of C1-OH producing dD-TAP.Several key genes involved in the biotransformation of thiamphenicol were predicted by integration analysis of multi-omic data. Among them, the GDH oxidoreductase （named capO2） carried by Hydrogenophaga borbori is the key enzyme responsible for the oxidation of the hydroxyl groups at C3 and C1 of thiamphenicol. The expression of the acetyltransferase gene carried by Thermomonas sp018242365 genus significantly increased during the rapid degradation of thiamphenicol, which was consistent with the generation rule of the acetylated product of thiamphenicol. Thus, Thermomonas sp018242365 inactivates thiamphenicol by C3-OH acetylation. The untargeted metabolomics method was used to reveal differential intracellular and extracellular metabolites. KEGG pathway enrichment analysis showed that thiamphenicol mainly affected metabolic pathways of steroid biosynthetic pathway, linoleic acid metabolic pathway, secondary bile acid biosynthesis, and biosynthesis of unsaturated fatty acid