Dysbiosis of Gut Microbiota by Environmental Pollutants: Implications for Host Health

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Novel Methods in Toxicology Research".

Deadline for manuscript submissions: closed (31 July 2022) | Viewed by 8700

Special Issue Editor


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Guest Editor
Institute of Hydrobiology, Chinese Academy of Science, Wuhan 430072, China
Interests: environmental behavior, toxicology, and molecular mechanisms of emerging pollutants; development of toxicity-ameliorative measures based on gut microbiota manipulation to protect the health of animals and humans
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Special Issue Information

Dear Colleagues,

There is accumulating evidence that verifies the fundamental roles of gut microbiota in the maintenance of host health and wellbeing. Alterations in the composition, diversity and metabolism of gut commensal microbes will compromise the physiological functions of host animals, ultimately leading to the pathogenesis of various diseases, including systemic inflammation, obesity, diabetes, and neurobehavioral disorders. It is notable that dynamics of the gut microbial community are susceptible to environmental stressors, especially toxic pollutants, which are potent to shift the gut microbiota and interrupt the physiological activities of hosts. However, the mechanisms and potential of environmental pollutants to shape the gut microbial community population remain less investigated. In particular, more effort is needed to establish the extrapolation of gut microbiome dysbiosis to host health, thereby providing a novel explanation about the mode of toxic action of environmental pollutants.

To this end, this Special Issue focuses on the original studies, reviews and short communications that are designed to explore the toxic effects of environmental pollutants on gut microbiota. Environmental pollutants include, but are not limited to, persistent organic pollutants, antibiotics, nanoparticles and metals. Research studies that are able to provide mechanistic insight into gut microbiota disturbances by pollutants and elucidate the underlying implications to host health are especially welcome.

Dr. Lianguo Chen
Guest Editor

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Keywords

  • gut microbiota
  • host health
  • environmental pollutants
  • gut–liver axis
  • gut–brain axis
  • mode of toxic action

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Published Papers (3 papers)

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Editorial

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2 pages, 149 KiB  
Editorial
Gut Microbiota Manipulation to Mitigate the Detrimental Effects of Environmental Pollutants
by Lianguo Chen
Toxics 2021, 9(6), 127; https://doi.org/10.3390/toxics9060127 - 1 Jun 2021
Cited by 19 | Viewed by 2674
Abstract
The ecotoxicology and human health risks of environmental pollutants are creating global concern, especially in the context of the prevalent and severe contamination of environmental abiotic and biotic compartments [...] Full article

Research

Jump to: Editorial

16 pages, 3937 KiB  
Article
Transcriptomic Interaction between Young Fecal Transplantation and Perfluorobutanesulfonate in Aged Zebrafish Gonads
by Lizhu Tang, Jing Li, Baili Sun, Yachen Bai, Xiangzhen Zhou and Lianguo Chen
Toxics 2022, 10(11), 631; https://doi.org/10.3390/toxics10110631 - 22 Oct 2022
Cited by 3 | Viewed by 2205
Abstract
The transfer of young fecal microbiota has been found to significantly refresh the reproductive endocrine system and effectively ameliorate the toxicity of perfluorobutanesulfonate (PFBS) in aged zebrafish recipients. However, the mechanisms underlying the antagonistic action of young fecal microbiota against the reproductive endocrine [...] Read more.
The transfer of young fecal microbiota has been found to significantly refresh the reproductive endocrine system and effectively ameliorate the toxicity of perfluorobutanesulfonate (PFBS) in aged zebrafish recipients. However, the mechanisms underlying the antagonistic action of young fecal microbiota against the reproductive endocrine toxicity of PFBS remain largely unknown. In this study, the aged zebrafish were transplanted with feces from young donors and then exposed to PFBS for 14 days. After exposure, the shift in the transcriptomic fingerprint of the gonads was profiled by using high-throughput sequencing, aiming to provide mechanistic clues into the interactive mode of action between young fecal transplantation and PFBS’s innate toxicity. The results showed that the gene transcription pattern associated with protein and lipid synthesis in the gonads of the aged individuals was quite different from the young counterparts. It was intriguing that the transplantation of young feces established a youth-like transcriptomic phenotype in the elderly recipients, thus attenuating the functional decline and maintaining a healthy aging state of the gonads. A sex specificity response was clearly observed. Compared to the aged females, more metabolic pathways (e.g., glycine, serine, and threonine metabolism; glyoxylate and dicarboxylate metabolism; pyrimidine metabolism) were significantly enriched in aged males receiving young feces transplants. PFBS dramatically altered the transcriptome of aged testes, while a much milder effect was observable in aged ovaries. Accordingly, a suite of biological processes related to germ cell proliferation were disrupted by PFBS in aged males, including the ECM–receptor interaction, retinol metabolism, and folate biosynthesis. In aged ovaries exposed to PFBS, mainly the fatty acid and arginine biosynthesis pathway was significantly affected. However, these transcriptomic disorders caused by PFBS were largely mitigated in aged gonads by transferring young feces. Overall, the present findings highlighted the potential of young fecal transplantation to prevent the functional compromise of gonads resulting from aging and PFBS. Full article
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11 pages, 2294 KiB  
Article
Sub-Chronic Difenoconazole Exposure Induced Gut Microbiota Dysbiosis in Mice
by Zhiwei Bao, Weitao Wang, Xiaofang Wang, Mingrong Qian and Yuanxiang Jin
Toxics 2022, 10(1), 34; https://doi.org/10.3390/toxics10010034 - 12 Jan 2022
Cited by 10 | Viewed by 2994
Abstract
Difenoconazole (DIF) is a widely separated triazole fungicide in many countries. The excessive usage of DIF increases the high volume of residues in agriculture production and water bodies. Some previous studies demonstrated the toxic effects of DIF on non-target animals, however, there were [...] Read more.
Difenoconazole (DIF) is a widely separated triazole fungicide in many countries. The excessive usage of DIF increases the high volume of residues in agriculture production and water bodies. Some previous studies demonstrated the toxic effects of DIF on non-target animals, however, there were still some gaps in the knowledge of the potential hazards of DIF to mammals and human health. Herein, 7-week-old male mice were exposed to 30 and 100 mg/kg/day DIF for 14 and 56 days. We observed that 56 days of DIF exposure decreased the colonic mucus expression of alcin blue-periodic acid-schiff (AB-PAS) stain and the immunochemical stain of muc2 protein. The transcript levels of mucin protein (muc1, muc2 and muc3) decreased significantly in the gut of mice followed 56 days of 100 mg/kg/day DIF exposure. In addition, the gut microbiota composition was also affected after 14 or 56 days of DIF exposure. Although the mucus expression after 14 days of DIF exposure only decreased slightly, the gut microbiota composition compared with the control group was changed significantly. Moreover, the DIF-30 and DIF-100 caused respectively different changes on the gut microbiota. The relative abundance of Bacteroidetes decreased significantly after 14 days and 56 days of DIF exposure. After 14 days of DIF exposure, there were 35 and 18 differential genera in the DIF-30 and DIF-100 group, respectively. There were 25 and 32 differential genera in the DIF-30 and DIF-100 group after 56 days of exposure, respectively. Meanwhile, the alpha diversity indexes, including observed species, Shannon, Simpson, Chao1 and ACE, in gut microbiota decreased significantly after 56 days of DIF exposure. Interestingly, the relative abundance of Akkermansia increased significantly after 56 days of 100 mg/kg/d DIF exposure. Although Akkermansia was considered as one probiotic, the phenomenon of dramatic Akkermansia increase with the decrease in gut microbiota diversity needed further discussion. These results provided some new insights on how DIF exposure impacts the mucus barrier and induces gut microbiota dysbiosis. Full article
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