Fig. 6: Pathways of NP-induced gut microbiota changes.

A The effects of NP treatment (1 × 10¹⁰ particles/mL) on the growth of various lactic acid bacteria (L. paracasei, L. acidophilus, and P. acidiloctici), Lachnospiraceae sp. (TSD-26; ATCC), and Ruminococcaceae sp. (TSD-27; ATCC). B Schematic of experimental process by interactions between bacterial EV and cell-derived EV. C Impact of Lachnospiraceae sp.-derived EV without or with NP treatment (1 × 10¹⁰ particles/mL) for 18 h on the growth of different bacterial species (L. paracasei, L. acidophilus, P. acidiloctici, and Ruminococcaceae sp.). D The impact of Ruminococcaceae sp.-derived EV without or with NP treatment (1 × 10¹⁰ particles/mL) for 44 h on the growth of different bacterial species (L. paracasei, L. acidophilus, P. acidiloctici, and Lachnospiraceae sp.). E Impact of goblet-like LS174T cells without or with NP treatment (10⁶ particles/mL) for 48 h on the growth of different bacterial species (L. paracasei, L. acidophilus, P. acidiloctici, and Lachnospiraceae sp. and Ruminococcaceae sp.). F Western blot of MUC13 inhibition by Lachnospiraceae sp.-derived EV. Data were shown as mean ± SD (n = 3) (* p value < 0.05). G Schematic representation summarizing the proposed mechanisms of NP-induced modulation of gut microbiota via EV. NP are taken up by Lachnospiraceae, whose EV suppress MUC13 expression in goblet cells. Concurrently, NP-modified EV from goblet cells promote the growth of Ruminococcaceae, collectively contributing to gut microbiota imbalance and potential intestinal barrier dysfunction.