Nanoplastics -Remodel gut microbiome, weaken intestinal defenses

Nanoplastics -Remodel gut microbiome, weaken intestinal defenses

Research shows how invisible nanoparticles manipulate cell phones and undermine your gut's delicate microbiome, raising new questions about the invisible health risks of environmental nanoplastics.

Study:Polystyrene nanoplastics disrupt the intestinal microenvironment by altering bacteria-host interactions through extracellular vesicle-delivered microRNAs. Photo credit: Sivstockstudio/Shutterstock.com

Exposure to polystyrene nanoplastics can disrupt gut health by altering interactions between bacteria and disrupting the gut microenvironment. A recently published study inNature communicationInvestigated how polystyrene nanoplastic exposure affects human health, focusing on bacteria-host interactions.

The effect of nanoplastic exposure on human health

People are frequently exposed to plastic fragments throughout the food chain, raising questions about their impact on the gut microbiome. The degradation of various types of plastics such as polystyrene (PS), polyvinyl chloride (PVC) and polyethylene (PE) leads to the development of microplastics (MP) and nanoplastics (NP).

Several studies have shown that MP or NP exposure can cause hematopoietic damage, liver injury and testicular disorders in mammals through intestinal dysbiosis. These studies have also shown that PS-MP and PE-MP exposure induce inflammation, immune imbalances, and intestinal barrier dysfunction. Specifically, PE-MP exposure alters gut microbial composition, favoring a selective increase in pathogenStaphylococcus aureus. This NP also promotes intestinal inflammation.

Despite the understanding of the toxic effects of MP and NP in humans, few studies have examined the interaction between microscopic plastics, gut microbiota and host. Furthermore, the underlying mechanism by which microscopic plastic affects human health remains relatively understudied.

Several studies have suggested that NPs are more harmful than MPS due to their smaller size. This allows them to penetrate tissues and organs and easily influence their biological functions. Understanding the precise pathway by which NPs cause gut dysbiosis and influence gut health is essential.

Extracellular vesicles (EVs) are tiny, membrane-bound lipid bilayer sacs released by animal cells and bacteria. These spherical structures carry diverse contents including DNA, RNAs, proteins and lipids. EVs play a crucial role in intercellular communication. Previous studies have shown that EVs often mediate the interaction between microbiota and intestinal epithelium and influence intestinal health and function.

About the study

The current study hypothesized that NP directly or indirectly influences microbiota composition through EVs. SeveralIn vivoAndin vitroExperiments were conducted to test this hypothesis. For example, the size and number of NPs used in this study were confirmed using nanoparticle tracking analysis (NTA).

Six-week-old male mice were exposed to fluorescently labeled NPs to examine their distribution in organs. Cellular uptake of NPs, serum biochemical analysis, real-time PCR and western blot were performed.

To understand how NP affects gut microbiota, microscopic polystyrene (100 nm) was orally administered to the mice four times a week for 12 weeks, specifically on days 1, 3, 5 and 7 of each week. A series of control mice not treated with NP were maintained as a reference.

Study results

The accumulation of NP (100 nm) was observed at different time points between 3 min and 48 h. In the current study, significant NP levels were found in the small intestine, liver, cecum, and colon of the study mice.

Oral NP exposure increased body weight compared to mice in the control group. However, the increase was moderate and was not associated with significant changes in white adipose tissue or liver weight. No significant changes in liver weight or white adipose tissue were observed. Intestinal shortening was not observed in NP-exposed mice, implying that intestinal bacteria and not inflammation were the primary target of NP-induced effects.

Biochemical analysis revealed that 12 weeks of NP exposure did not significantly modify serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), creatinine (CRE), or blood urea nitrogen (BUN). This finding suggests that the gut microbiota and barrier can be directly influenced by NP.

In the current study, it was found that NP could penetrate into the enterocyte-like differentiated Caco-2 cells and mouse intestine after 24 hours of treatment. After entry, it reduces the expression of tight junction proteins, including zonula occludens-1 (ZO-1) and occludins (OCC). This disorder causes characteristic intestinal damage, including increased intestinal permeability or leaky gut.

Gene Ontology (GO) analysis showed that NP exposure significantly altered the mice's intestinal gene expression and metabolic functions. Principal component analysis (PCA) of microRNA (miRNA) diversity in mouse feces revealed that NP exposure significantly modified miRNA profiles and reduced the diversity of specific miRNAs. Further in-depth analysis discovered the role of miRNAs as regulators of primary physiological functions, particularly those associated with intestinal cell junctions.

Experimental findings suggest that NP could disrupt the expression of the tight junction proteins by regulating miRNAs in intestinal cells, which ultimately disrupts the intestinal environment. Predictive analysis showed that NP exposure affected miRNAs such as AS-MIR-98-3P, HAS-MIR-548H-3P, HAS-MIR-548Z, HAS-MIR-548D-3P, HAS-MIR-548AZ-5P, HAS-MIR-12136 and HAS-MIR-MIR-3P expression on the ZO-101-MIR-3P expression regulated.

Furthermore, the study found that NP exposure increased the expression of mouse-specific miRNAs such as MMU-MIR-501-3p and MMU-MIR-700-5p, which also disrupt the expression of ZO-1 and MUC-13.

Immunocytochemistry (ICC), qPCR and Western blot analysis revealed that NP treatment decreased MUC-13 expression in mice and enterocyte-like differentiated Caco-2 cells.

With prolonged NP exposure, unique bacterial species initially increased and decreased. The most notable effect was a shift in the relative abundance of specific bacterial taxa, rather than a simple loss of overall diversity. For example, Lactobacillaceae decreased and Ruminococcaceae increased.

The study also found that Akkermansia, a next-generation probiotic bacteria, increased abundance in NP-exposed mice, particularly at later times. Experimental findings showed that the influence of NP on the gut microbiome was not directly caused by NP toxicity but by other mechanisms.

Specifically, the study shows that the changes were mediated by extracellular vesicles (EVs) derived from intestinal cells and certain bacteria instead of the direct toxic effects of NP on bacterial growth.LachnospiraceaeOf those from SP. derived EVs did not affect the growth of intestinal bacteria.

The novelty of this study lies in the discovery of a specific mechanism. NP alters the intestinal microenvironment by modulating EV-mediated delivery of miRNAs, which then disrupt the intestinal barrier and selectively influence the growth of bacterial taxa. This represents a newly described pathway in the context of NP toxicity.

Conclusions

The current study proposed that NP includes certain bacterial taxa includingLachnospiraceaeAndRuminococcaceae. The alteration of the gut microbiome upon NP exposure is mediated by host-microbiota interactions through EV. NP was taken up by Lachnospiraceae, which triggered suppressed mucin-13 expression.

Additionally, EVs released from kauflet-like cells after NP exposure promoted the growth ofRuminococcaceaePresentHighlighting a complex interplay between derived and bacterial vesicles.

Further research into the effects of NPs on human and environmental health is needed. While these results provide new insights into how NP can disrupt gut health, it is important to note that the experiments were conducted in mice. The relevance of the doses and findings to typical human exposures remains to be determined.

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