Using inoculum from a microcosm study that exhibited aerobic transformation of cis-1,2-dichloroethene (cDCE) and trichloroethene (TCE) commensurate with biodegradation of monoaromatic compounds, enrichment cultures were developed by providing benzene, chlorobenzene (CB), dichlorobenzene (DCB) isomers and 1,2,4-trichlorobenzene as carbon and energy sources. Isolates that grow on benzene, CB, 1,2-DCB and 1,3-DCB were identified as Rhodococcus, Ralstonia, Variovorax and Ralstonia spp., respectively. Cometabolic transformation of cDCE and TCE by resting cells was demonstrated. Transformation capacities (T(c)=0.47-1.0 μg TCE mg(-1)biomass; 1.3-5.3 μg cDCE mg(-1)biomass), transformation yields (T(y)=0.18-0.27 μg TCE mg(-1)substrate; 0.46-2.1 μg cDCE mg(-1)substrate), and pseudo-first-order cometabolic degradation rate constants (0.00081-0.0031 L mg TCE(-1)d(-1); 0.0012-0.030 L mg cDCE(-1)d(-1)) for resting cells grown on benzene, CB, 1,2-DCB and 1,3-DCB were generally lower in comparison to phenol and toluene-grown isolates. Cometabolic transformation of cDCE and TCE also occurred while the cultures concurrently consumed their growth substrate (T(c)(')=0.15-0.33 μg TCE mg(-1)biomass; 4.9-11 μg cDCE mg(-1)biomass; T(y)(')=0.06-0.11 μg TCE mg(-1)substrate; 1.7-4.6 μg cDCE mg(-1)substrate), a condition that is more likely to be encountered in situ compared to cometabolic transformations by resting cells. This study is the first to report transformation rates, capacities, and yields for cometabolism of cDCE and TCE during aerobic growth on benzene, CB, 1,2-DCB and 1,3-DCB. This type of information is needed to predict the potential for natural attenuation when these compounds occur as co-contaminants.
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http://dx.doi.org/10.1016/j.chemosphere.2011.04.007 | DOI Listing |
Immunity
December 2020
Division of Immunology, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA. Electronic address:
The mechanisms by which regulatory T (Treg) cells differentially control allergic and autoimmune responses remain unclear. We show that Treg cells in food allergy (FA) had decreased expression of transforming growth factor beta 1 (TGF-β1) because of interleukin-4 (IL-4)- and signal transducer and activator of transciription-6 (STAT6)-dependent inhibition of Tgfb1 transcription. These changes were modeled by Treg cell-specific Tgfb1 monoallelic inactivation, which induced allergic dysregulation by impairing microbiota-dependent retinoic acid receptor-related orphan receptor gamma t (ROR-γt) Treg cell differentiation.
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