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• W4308209712 abstract "Vol. 130, No. 11 Invited PerspectiveOpen AccessInvited Perspective: PFOS–Pick Fiber, Oust Sulfonateis accompanied byMetabolomic, Lipidomic, Transcriptomic, and Metagenomic Analyses in Mice Exposed to PFOS and Fed Soluble and Insoluble Dietary Fibers Rachel M. Golonka and Matam Vijay-Kumar Rachel M. Golonka Department of Physiology and Pharmacology, University of Toledo College of Medicine and Life Sciences, Toledo, Ohio, USA Search for more papers by this author and Matam Vijay-Kumar Address correspondence to Matam Vijay-Kumar, Department of Physiology and Pharmacology, University of Toledo College of Medicine and Life Sciences, Toledo OH 43614 USA. Telephone: (419) 383-4130. Email: E-mail Address: [email protected] https://orcid.org/0000-0002-8732-0167 Department of Physiology and Pharmacology, University of Toledo College of Medicine and Life Sciences, Toledo, Ohio, USA Search for more papers by this author Published:4 November 2022CID: 111301https://doi.org/10.1289/EHP12012AboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit As residents of Toledo, Ohio—a city that neighbors Flint, Michigan, and lies along Lake Erie, with its frequent algal blooms—we deeply appreciate both the critical importance of clean, safe drinking water and the complexity of remediating and preventing contamination. Cooperative actions of prevention include researching the data gaps, developing safe alternatives of the toxic agent, mitigating the release of chemicals into the environment, and raising awareness to the public and policy holders.1 These implemented plans have been useful in reducing contamination of many toxicants, but some agents, such as per- and polyfluoroalkyl substances (PFAS), have been overlooked for several reasons, including from inadequate assessment of their exposure level in the environment.1,2 Of other concern, preventing contamination events may help only so much for those who have been previously exposed to a toxic chemical. We reason this to be true when considering that many chemicals grouped under PFAS have long half-lives that range from 3 to 5 y after exposure.3,4 Other evidence to support our notion is from epidemiological studies that have uncovered environmental toxicants, such as PFAS, to cause adverse health outcomes that can vary based on their toxicokinetic properties.5 Altogether, we believe one of the main goals to preventing detrimental side effects of toxic exposures should be to determine a clinical intervention that can enable individuals to metabolize and excrete the agent more quickly.A recent, elegant study by Deng et al. provides a step toward this goal by identifying a potential dietary intervention to mitigate the adverse effects of perfluorooctane sulfonate (PFOS).6 PFOS is the most common of the PFAS and can contaminate both drinking water and food, such as fish and vegetables.7,8 For perspective, a recent 2016 report determined that drinking water supplied to 6 million U.S. residents was contaminated with PFOS at levels (>70 ng/L) exceeding the U.S. Environmental Protection Agency’s lifetime health advisory for PFOS exposure.9 The National Health and Nutrition Examination Survey also found that individuals ≥12 years of age who consumed even small amounts of fish had a 10%–20% increase in PFOS levels when compared with nonconsumers.10 Oral exposure to PFOS can result in several health consequences, including a severe imbalance and alterations in the gut microbial community, that is, microbiota dysbiosis, as demonstrated in mouse and zebrafish models.11 Other pathologies following PFOS exposure that could be a sequel of gut microbiota dysbiosis encompass hepatic inflammation and steatosis.12–14 There are only a few reports that nutritional agents, such as curcumin15 and vitamin C,16 protect against PFOS by alleviating hepatic inflammation; these reports are typically observed in rodent models. Of note, one study reported that a probiotic cocktail of lactic acid bacteria can revert both gut and liver damage induced by PFOS in mice.7Given that gut microbiota dysbiosis is a consequence of PFOS and could be the cause of other intestinal and liver damage following PFOS exposure, interventions that target the gut microbiota would be clinically relevant. Following this concept, Deng et al. pieced together two key findings from the literature: a) ablating or reshaping the gut microbiota by antibiotic treatment or fecal microbiota transplantation, respectively, alleviated PFOS-induced hepatotoxicity in mice,17 and b) self-reported high intake of dietary fiber was associated with a lower serum concentration of PFOS.18 Dietary fibers are plant-derived complex carbohydrates with prebiotic properties that nourish the gut bacteria by their fermentation into short-chain fatty acids. Together, these studies provided a strong rationale for Deng et al. to test fermentable fibers such as inulin (polyfructosan) and pectin (polygalacturonate) as a plausible therapy to abate PFOS accumulation and the related adverse effects in mice. Indeed, the authors found dietary inulin, and to a lesser degree, pectin, corrected fecal microbiota dysbiosis detected in PFOS-exposed animals. The restoration of the fecal microbiota profile may have contributed to the observed mitigation of PFOS-induced liver pathology following dietary fiber intervention, but more studies are required to affirm this possible mechanistic link. Using an integrated multi-omics approach, Deng et al. delineated that the protective effects of dietary inulin resulted from lowering the PFOS-induced increase in hepatic ceramides and sphingolipids, molecules associated with metabolic dysfunction.Previous studies have supported the notion that inulin has predominant effects in promoting health when compared with other fermentable fibers, such as pectin, but recent evidence now shows an irony of extremes. Dietary inulin can either substantially alleviate or deteriorate health conditions, and which end of the spectrum is observed depends on the context of disease. In contrast to the report by Deng et al., which highlights inulin as helpful against PFOS, our prior reports demonstrated inulin to be very harmful in mice with inflammatory bowel disease, whereas pectin rescued them from disease.19,20 We believe this disparity is probably attributed to an unevenness in fiber fermentation, as well as to the production of short-chain fatty acids and their utilization via cross-feeding among themselves by gut microbiota in different disease conditions. The disproportion in fiber fermentation would then contribute to an overwhelming and endless possibility of gut microbiota signatures for each pathology, making it impossible to label individual bacterial species as either universally good or universally bad. Accordingly, the distinct effects of dietary fiber reinforce the concept that not every intervention can be repurposed as a new treatment for another disease. In the context of PFOS, though, inulin, and to a slight degree, pectin, have some possible advantage in restoring eubiosis, or balance, in gut microbiota homeostasis and reducing liver damage caused by PFOS. Subsequent studies are warranted to verify these dietary fermentable fibers as clinically relevant interventions.Although introducing more dietary fiber into the diet could be favorable for mitigating the effects of PFOS, individuals are unique in terms of their health history, including their personalized gut microbiota profile and their nutritional requirements; therefore, everyone may respond differently to inulin, pectin, or both. We would not find it surprising to consider the probable large number of unreported cases for gut microbiota dysbiosis co-occurring with preexisting liver diseases, as well as the potential of PFOS exposure to exacerbate the disease. How the gut microbiota would further shift in this situation is unclear but we believe it would vary greatly from person to person because of genetics, immune status, and dietary habits. Even with these variables to complicate the scenario, pattern shifts in bacterial species at the phyla or taxonomical level may still be common, irrespective of the starting gut microbiota profile, supporting the idea of measuring gut microbiota composition as a potential diagnostic tool for PFOS exposure. However, more studies are required to define consistent changes in the gut microbiota after PFOS exposure. The source of dietary fiber adds another layer of complexity given that highly refined fiber(s) may have lost some nutritional value during the processing of natural whole foods. Nevertheless, Deng et al. do provide promising groundwork for dietary fermentable fiber as a potential single entity to combat two major PFOS consequences. This study thus reemphasizes the notion that we are not only what we eat, but also what our gut microbiota eat.References1. Ritscher A, Wang Z, Scheringer M, Boucher JM, Ahrens L, Berger U, et al.2018. Zurich statement on future actions on per- and polyfluoroalkyl substances (PFASs). Environ Health Perspect 126(8):84502, PMID: 30235423, 10.1289/EHP4158. Link, Google Scholar2. Sunderland EM, Hu XC, Dassuncao C, Tokranov AK, Wagner CC, Allen JG. 2019. A review of the pathways of human exposure to poly- and perfluoroalkyl substances (PFASs) and present understanding of health effects. J Expo Sci Environ Epidemiol 29(2):131–147, PMID: 30470793, 10.1038/s41370-018-0094-1. Crossref, Medline, Google Scholar3. Li Y, Fletcher T, Mucs D, Scott K, Lindh CH, Tallving P, et al.2018. Half-lives of PFOS, PFHxS and PFOA after end of exposure to contaminated drinking water. Occup Environ Med 75(1):46–51, PMID: 29133598, 10.1136/oemed-2017-104651. Crossref, Medline, Google Scholar4. 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J Appl Toxicol 42(5):806–817, PMID: 34687223, 10.1002/jat.4258. Crossref, Medline, Google Scholar14. Wang Q, Huang J, Liu S, Wang C, Jin Y, Lai H, et al.2022. Aberrant hepatic lipid metabolism associated with gut microbiota dysbiosis triggers hepatotoxicity of novel PFOS alternatives in adult zebrafish. Environ Int 166:107351, PMID: 35738203, 10.1016/j.envint.2022.107351. Crossref, Medline, Google Scholar15. Eke D, Çelik A, Yilmaz MB, Aras N, Kocatürk Sel S, Alptekin D. 2017. Apoptotic gene expression profiles and DNA damage levels in rat liver treated with perfluorooctane sulfonate and protective role of curcumin. Int J Biol Macromol 104(pt A):515–520, PMID: 28634058, 10.1016/j.ijbiomac.2017.06.075. Crossref, Medline, Google Scholar16. Su M, Liang X, Xu X, Wu X, Yang B. 2019. Hepatoprotective benefits of vitamin C against perfluorooctane sulfonate-induced liver damage in mice through suppressing inflammatory reaction and ER stress. Environ Toxicol Pharmacol 65:60–65, PMID: 30551094, 10.1016/j.etap.2018.12.004. Crossref, Medline, Google Scholar17. Jiang L, Hong Y, Xiao P, Wang X, Zhang J, Liu E, et al.2022. The role of fecal microbiota in liver toxicity induced by perfluorooctane sulfonate in male and female mice. Environ Health Perspect 130(6):67009, PMID: 35759388, 10.1289/EHP10281. Link, Google Scholar18. Dzierlenga MW, Keast DR, Longnecker MP. 2021. The concentration of several perfluoroalkyl acids in serum appears to be reduced by dietary fiber. Environ Int 146:106292, PMID: 33395939, 10.1016/j.envint.2020.106292. Crossref, Medline, Google Scholar19. Singh V, Yeoh BS, Walker RE, Xiao X, Saha P, Golonka RM, et al.2019. Microbiota fermentation-NLRP3 axis shapes the impact of dietary fibres on intestinal inflammation. Gut 68(10):1801–1812, PMID: 30670576, 10.1136/gutjnl-2018-316250. Crossref, Medline, Google Scholar20. Miles JP, Zou J, Kumar MV, Pellizzon M, Ulman E, Ricci M, et al.2017. Supplementation of low- and high-fat diets with fermentable fiber exacerbates severity of DSS-induced acute colitis. Inflamm Bowel Dis 23(7):1133–1143, PMID: 28590342, 10.1097/MIB.0000000000001155. Crossref, Medline, Google ScholarThe authors declare they have nothing to disclose.FiguresReferencesRelatedDetailsRelated articlesMetabolomic, Lipidomic, Transcriptomic, and Metagenomic Analyses in Mice Exposed to PFOS and Fed Soluble and Insoluble Dietary Fibers4 November 2022Environmental Health Perspectives Vol. 130, No. 11 November 2022Metrics About Article Metrics Publication History Manuscript received17 August 2022Manuscript revised24 September 2022Manuscript accepted28 September 2022Originally published4 November 2022 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days." @default.
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