Impact of microplastics on the intestinal microbiota: A systematic review of preclinical evidence

We systematically review the in vivo preclinical evidence on the impact of microplastics (MPs) on the intestinal microbiota and morphofunctional changes involving the intestinal mucosa. By using a comprehensive and structured search in electronic databases 28 original studies were recovered and analyzed. Zebrafish and mice were the main animal models, while the dose and shape of MPs used were quite heterogeneous. Studies show that MPs are potential triggers of intestinal dysbiosis, which has been characterized by enrichment of Firmicutes, Proteobacteria and Chlamydia. Conversely, there was a reduction in Bacteroidetes phylum abundance. By trapping and stimulating intestinal inflammatory infiltrate, exposure to MPs increased intestinal permeability and the expression of immune signatures associated with inflammation, such as IL-1α, IL-1β, TNF-α, IFN-γ and IL-6. Thus, current evidence supports potential inflammatory and dysbiotic properties of MPs. In addition, the data indicate that MPs can display structural changes secondary to exposure to MPs. Analysis of methodological quality indicated that current preclinical evidence is at high risk of bias. We hope that controlling that bias sources described in this systematic review will be useful to improve the quality of reports. Microplastics disrupt the intestinal microbiota and make the intestinal mucosa hyper-responsive. (A) Animals fed with control diet (without microplastics); (B) animals fed with diet containing MP, which had enrichment of Firmicutes, Verrumicrobia, Proteobacteria and Chamydiae phylum, thinning mucus layer and increases on the intestinal permeability and inflammation. TL: T-Lymphocytes; BL: B-Lymphocytes; DC: Dendritic cells; MФ: Macrophages; Ig: Immunoglobulin; GC: Goblet cell; IEC: Intestinal enterocyte cell; IL: Interleukin; TNF: Tumor Necrosis Factor; CAT: Catalase; DAO: Diamine oxidase; TLR: Toll-like receptor; MP: Microplastic. [Display omitted]