Multi-omics reveals that Bifidobacterium breve M-16V may alleviate the immune dysregulation caused by nanopolystyrene

There is a growing attention regarding the toxic effect of microplastics pollutants. However, comprehensive phenotyping-and omics-based strategies for the toxicity evaluation of microplastics on the host remain to be established. To this end, we designed an encompassing phenotyping and multi-omics analysis method to detect the molecular interference of nanopolystyrene (PS)-exposed mice. The exposure time was 28 days with 1000 mu g/ L PS. We found that PS induced microbial alteration and metabolic disorders, which was closely related to immune disturbances. In addition, the altered expression of some genes related to immune dysregulation was observed. Interestingly, Bifidobacterium breve M-16V (B. breve M-16V) significantly inhibited Th2 and Th17 lymphocyte subset. Simultaneously, B.breve M-16V may activate MyD88 expression and promote Th1-related cytokine IL-12 production. In addition, B. breve M-16V may partially restore the gut microbiota dysbiosis. In summary, we demonstrated that the combined phenotyping and omics-based profiling established a practical framework that allowed us to gain a deeper understanding of the maladaptive consequences of PS exposure. It can be utilized to evaluate the toxicity of other environmental microplastics pollutants. Meanwhile, we found that B. breve M-16V has certain anti-inflammatory and immunomodulatory functions through host-microbiome interactions.

Automated summary

This study established a comprehensive phenotyping and multi-omics analysis method to evaluate the toxicity of nanopolystyrene (PS) on mice. The results showed that PS exposure caused microbial alteration, metabolic disorders, and immune disturbances. Additionally, the probiotic Bifidobacterium breve M-16V was found to have anti-inflammatory and immunomodulatory effects through host-microbiome interactions.