Microcystin-LR (MC-LR) and microcystin-RR (MC-RR) are the two most common microcystins (MCs) present in fresh water posing a direct threat to public health because of their hepatotoxicity. A novel MC-degrading bacterium designated MC-LTH1 capable of degrading MC-LR and -RR was isolated, and the degradation rates and mechanisms of MC-LR and -RR for this bacterium were investigated. The bacterium was identified as Bordetella sp. and shown to possess a homologous mlrA gene responsible for degrading MCs. To the best of our knowledge, this is the first report of mlrA gene detection in Bordetella species. MC-LR and -RR were completely degraded separately at rates of 0.31 mg/(L h) and 0.17 mg/(L h). However, the degradation rates of MC-LR and -RR decreased surprisingly to 0.27 mg/(L h) and 0.12 mg/(L h), respectively, when both of them were simultaneously present. Degradation products were identified by high performance liquid chromatography coupled with time-of-flight mass spectrometry. Adda (m/z 332.2215, C20H29NO3) commonly known as a final product of MC degradation by isolated bacteria was detected as an intermediate in this study. Linearized MC-LR (m/z 1013.5638, C49H76N10O13), linearized MC-RR (m/z 1056.4970, C49H77N13O13), and tetrapeptide (m/z 615.3394, C32H46N4O8) were also detected as intermediates. These results indicate that the bacterial strain MC-LTH1 is quite efficient for the detoxification of MC-LR and MC-RR, and possesses significant bioremediation potential.
BackgroundIL‐37 has been identified as a fundamental inhibitor of inflammatory and immunity responses. It plays a crucial protective role in several cancers, but its anti‐tumor activity and the potential regulatory mechanism of IL‐37 in non‐small cell lung cancer (NSCLC) is largely unclear.MethodsEnzyme‐linked immunosorbent assay was used to detect plasma IL‐37 expression in NSCLC patients and healthy controls. The NSCLC cell line A549 was cultured with recombinant human IL‐37 or recombinant human IL‐6 protein. A549 invasion and metastasis were detected using Transwell invasion and scratch wound healing assays, respectively. Protein expression of STAT3, pSTAT3, E‐cadherin, vimentin, and N‐cadherin were detected using Western blotting, and messenger RNA expression of STAT3, E‐cadherin, vimentin, and N‐cadherin was assessed in each group using real time PCR.ResultsIL‐37 plasma expression was decreased in NSCLC patients, and the downregulation of IL‐37 was correlated with tumor stage. In vitro, IL‐37 inhibited invasion and migration in A549 cells, while IL‐6 promoted invasion and migration in A549 cells. pSTAT3, vimentin, and N‐cadherin expression was increased. E‐cadherin expression was lower in the IL‐6 group than in the control group; however, the opposite pattern was observed in the IL‐37 + IL‐6 group.ConclusionOur results showed that IL‐37 plays an inhibitory role in NSCLC progression, possibly by suppressing STAT3 activation and decreasing epithelial‐to‐mesenchymal transition by inhibiting IL‐6 expression. IL‐37 could serve as a potential novel tumor suppressor in NSCLC.
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