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Anthropogenic organohalide pollutants pose a severe threat to public health and ecosystems. In situbioremediation using organohalide respiring bacteria (OHRB) offers an environmentally friendly and cost-efficient strategy for decontaminating organohalide-polluted sites. The genomic structures of many OHRB suggest that dehalogenation traits can be horizontally transferred among microbial populations, but their occurrence among anaerobic OHRB has not yet been demonstrated experimentally. This study isolates and characterizes a novel tetrachloroethene (PCE)-dechlorinating Sulfurospirillumsp. strain SP, distinguishing itself among anaerobic OHRB by showcasing a mechanism essential for horizontal dissemination of reductive dehalogenation capabilities within microbial populations. Its genetic characterization identifies a unique plasmid (pSULSP), harboring reductive dehalogenase and de novocorrinoid biosynthesis operons, functions critical to organohalide respiration, flanked by mobile elements. The active mobility of these elements was demonstrated through genetic analyses of spontaneously emerging nondehalogenating variants of strain SP. More importantly, bioaugmentation of nondehalogenating microcosms with pSULSP DNA triggered anaerobic PCE dechlorination in taxonomically diverse bacterial populations. Our results directly support the hypothesis that exposure to anthropogenic organohalide pollutants can drive the emergence of dehalogenating microbial populations via horizontal gene transfer and demonstrate a mechanism by which genetic bioaugmentation for remediation of organohalide pollutants could be achieved in anaerobic environments.

Organohalide pollutants are prevalent in coastal regions due to extensive intervention by anthropogenic activities, threatening public health and ecosystems. Gradients in salinity are a natural feature of coasts, but their impacts on the environmental fate of organohalides and the underlying microbial communities remain poorly understood. Here we report the effects of salinity on microbial reductive dechlorination of tetrachloroethene (PCE) and polychlorinated biphenyls (PCBs) in consortia derived from distinct environments (freshwater and marine sediments). Marine-derived microcosms exhibited higher halotolerance during PCE and PCB dechlorination, and a halotolerant dechlorinating culture was enriched from these microcosms. The organohalide-respiring bacteria (OHRB) responsible for PCE and PCB dechlorination in marine microcosms shifted from Dehalococcoidesto Dehalobiumwhen salinity increased. Broadly, lower microbial diversity, simpler co-occurrence networks, and more deterministic microbial community assemblages were observed under higher salinity. Separately, we observed that inhibition of dechlorination by high salinity could be attributed to suppressed viability of Dehalococcoidesrather than reduced provision of substrates by syntrophic microorganisms. Additionally, the high activity of PCE dechlorinating reductive dehalogenases (RDases) in in vitro tests under high salinity suggests that high salinity likely disrupted cellular components other than RDases in Dehalococcoides. Genomic analyses indicated that the capability of Dehalobiumto perform dehalogenation under high salinity was likely owing to the presence of genes associated with halotolerance in its genomes. Collectively, these mechanistic and ecological insights contribute to understanding the fate and bioremediation of organohalide pollutants in environments with changing salinity.

Organohalide pollutants are prevalent in coastal regions due to extensive intervention by anthropogenic activities, threatening public health and ecosystems. Gradients in salinity are a natural feature of coasts, but their impacts on the environmental fate of organohalides and the underlying microbial communities remain poorly understood. Here we report the effects of salinity on microbial reductive dechlorination of tetrachloroethene (PCE) and polychlorinated biphenyls (PCBs) in consortia derived from distinct environments (freshwater and marine sediments). Marine-derived microcosms exhibited higher halotolerance during PCE and PCB dechlorination, and a halotolerant dechlorinating culture was enriched from these microcosms. The organohalide-respiring bacteria (OHRB) responsible for PCE and PCB dechlorination in marine microcosms shifted from Dehalococcoidesto Dehalobiumwhen salinity increased. Broadly, lower microbial diversity, simpler co-occurrence networks, and more deterministic microbial community assemblages were observed under higher salinity. Separately, we observed that inhibition of dechlorination by high salinity could be attributed to suppressed viability of Dehalococcoidesrather than reduced provision of substrates by syntrophic microorganisms. Additionally, the high activity of PCE dechlorinating reductive dehalogenases (RDases) in in vitro tests under high salinity suggests that high salinity likely disrupted cellular components other than RDases in Dehalococcoides. Genomic analyses indicated that the capability of Dehalobiumto perform dehalogenation under high salinity was likely owing to the presence of genes associated with halotolerance in its genomes. Collectively, these mechanistic and ecological insights contribute to understanding the fate and bioremediation of organohalide pollutants in environments with changing salinity.Graphical Abstract

Widespread polybrominated diphenyl ethers (PBDEs) contamination poses risks to human health and ecosystems. Bioremediation is widely considered to be a less ecologically disruptive strategy for remediation of organohalide contamination, but bioremediation of PBDE-contaminated sites is limited by a lack of knowledge about PBDE-dehalogenating microbial populations. Here we report anaerobic PBDE debromination in microcosms established from geographically distinct e-waste recycling sites. Complete debromination of a penta-BDE mixture to diphenyl ether was detected in 16 of 24 investigated microcosms; further enrichment of these 16 microcosms implicated microbial populations belonging to the bacterial genera Dehalococcoides, Dehalogenimonas, and Dehalobacterin PBDE debromination. Debrominating microcosms tended to contain either both Dehalogenimonasand Dehalobacteror Dehalococcoidesalone. Separately, complete debromination of a penta-BDE mixture was also observed by axenic cultures of Dehalococcoides mccartyistrains CG1, CG4, and 11a5, suggesting that this phenotype may be fairly common amongst Dehalococcoides. PBDE debromination in these isolates was mediated by four reductive dehalogenases not previously known to debrominate PBDEs. Debromination of an octa-BDE mixture was less prevalent and less complete in microcosms. The PBDE reductive dehalogenase homologous genes in Dehalococcoidesgenomes represent plausible molecular markers to predict PBDE debromination in microbial communities via their prevalence and transcriptions analysis.

Widespread polybrominated diphenyl ethers (PBDEs) contamination poses risks to human health and ecosystems. Bioremediation is widely considered to be a less ecologically disruptive strategy for remediation of organohalide contamination, but bioremediation of PBDE-contaminated sites is limited by a lack of knowledge about PBDE-dehalogenating microbial populations. Here we report anaerobic PBDE debromination in microcosms established from geographically distinct e-waste recycling sites. Complete debromination of a penta-BDE mixture to diphenyl ether was detected in 16 of 24 investigated microcosms; further enrichment of these 16 microcosms implicated microbial populations belonging to the bacterial genera Dehalococcoides, Dehalogenimonas, and Dehalobacterin PBDE debromination. Debrominating microcosms tended to contain either both Dehalogenimonasand Dehalobacteror Dehalococcoidesalone. Separately, complete debromination of a penta-BDE mixture was also observed by axenic cultures of Dehalococcoides mccartyistrains CG1, CG4, and 11a5, suggesting that this phenotype may be fairly common amongst Dehalococcoides. PBDE debromination in these isolates was mediated by four reductive dehalogenases not previously known to debrominate PBDEs. Debromination of an octa-BDE mixture was less prevalent and less complete in microcosms. The PBDE reductive dehalogenase homologous genes in Dehalococcoidesgenomes represent plausible molecular markers to predict PBDE debromination in microbial communities via their prevalence and transcriptions analysis.

Halogenated flame retardants (HFRs) have been extensively used in various consumer products and many are classified as persistent organic pollutants due to their resistance to degradation, bioaccumulation potential and toxicity. HFRs have been widely detected in the municipal wastewater and wastewater treatment solids in wastewater treatment plants (WWTPs), the discharge and agricultural application of which represent a primary source of environmental HFRs contamination. This review seeks to provide a current overview on the occurrence, fate, and impacts of HFRs in WWTPs around the globe. We first summarize studies recording the occurrence of representative HFRs in wastewater and wastewater treatment solids, revealing temporal and geographical trends in HFRs distribution. Then, the efficiency and mechanism of HFRs removal by biosorption, which is known to be the primary process for HFRs removal from wastewater, during biological wastewater treatment processes, are discussed. Transformation of HFRs via abiotic and biotic processes in laboratory tests and full-scale WWTPs is reviewed with particular emphasis on the transformation pathways and functional microorganisms responsible for HFRs biotransformation. Finally, the potential impacts of HFRs on reactor performance (i.e., nitrogen removal and methanogenesis) and microbiome in bioreactors are discussed. This review aims to advance our understanding of the fate and impacts of HFRs in WWTPs and shed light on important questions warranting further investigation.

Cocontamination by chloroform and chloroethenes often confounds bioremediation efforts. Here, we describe Dehalococcoides mccartyistrain GEO12 that dechlorinates trichloroethene to ethene in 14 μM (1.6 mg·L–1) chloroform. The same chloroform concentration effectively inhibited dechlorination in Dehalococcoidesstrains ANAS2, 11a, and BAV1. Successive transfers of strain GEO12 in increasing concentrations of chloroform led to culture GEO12CF that tolerated 83 μM (10 mg·L–1) chloroform. The genome of strain GEO12 revealed seven reductive dehalogenase homologous (rdh) genes, including tceAand vcrA. Transcriptional analyses showed that chloroform (45 μM; 5.3 mg·L–1) in culture GEO12CF enhanced the transcription of tceAto a statistically significant degree (the median increase was 55.4 transcripts per 10416S rRNA, CI95%= [12.9, 125]). The increase of vcrAtranscripts in the presence of chloroform (45 μM; 5.3 mg·L–1) in culture GEO12CF was not statistically significant because the CI95%range spanned 0 (the median increase was 109 transcripts per 10416S rRNA, CI95%= [−13.6, 246]). Inhibition of dehalogenation by chloroform is often seen in Dehalococcoides, but the mechanism remains unknown. Our results suggest that culture GEO12CF may overcome chloroform inhibition by rdhupregulation. The chloroform-adapted culture GEO12CF provides insights into the metabolic flexibility of Dehalococcoidesand could be used to fight chloroethene contamination where chloroform is a cocontaminant.

Respiratory syncytial virus–bronchiolitis is a major independent risk factor for subsequent asthma, but the causal mechanisms remain obscure. We identified that transient plasmacytoid dendritic cell (pDC) depletion during primary Pneumovirus infection alone predisposed to severe bronchiolitis in early life and subsequent asthma in later life after reinfection. pDC depletion ablated interferon production and increased viral load; however, the heightened immunopathology and susceptibility to subsequent asthma stemmed from a failure to expand functional neuropilin-1+ regulatory T (T reg) cells in the absence of pDC-derived semaphorin 4a (Sema4a). In adult mice, pDC depletion predisposed to severe bronchiolitis only after antibiotic treatment. Consistent with a protective role for the microbiome, treatment of pDC-depleted neonates with the microbial-derived metabolite propionate promoted Sema4a-dependent T reg cell expansion, ameliorating both diseases. In children with viral bronchiolitis, nasal propionate levels were decreased and correlated with an IL-6high/IL-10low microenvironment. We highlight a common but age-related Sema4a-mediated pathway by which pDCs and microbial colonization induce T reg cell expansion to protect against severe bronchiolitis and subsequent asthma.