Correction: Perinatal foodborne titanium dioxide exposure-mediated dysbiosis predisposes mice to develop colitis through life

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Originally At days 50 after birth, TiO 2 exposure only increased the level of Muc2 (Additional file 5: Fig. S5A-C) At days 50 after birth, TiO 2 exposure only increased the level of Muc2 (Additional file 5: Fig. S5A, E) At days 50 after birth, TiO 2 exposure only increased the level of Muc2 (Additional file 5: Fig. S5A) Since perinatal exposure to TiO 2 altered the functionality of the colonic epithelium, we then monitored its effects on the intestinal epithelial stem cells (IESC) homeostasis (Fig. 3D-F; Additional file 5: Fig. S3D-F) Since perinatal exposure to TiO 2 altered the functionality of the colonic epithelium, we then monitored its effects on the intestinal epithelial stem cells (IESC) homeostasis (Fig. 4D-F; Additional file 5: Fig. S4D-F)

Section Originally published text Corrected text
At day 50, mice exposed to TiO 2 had an increased mRNA levels of colonic CD44, Leucine-rich repeatcontaining G-protein coupled receptor 5 (Lgr5), Achaete-scute complex homolog 2 (Ascl2) and Musashi RNA-binding protein 1 (Musashi), three markers of CBC, Telomerase reverse transcriptase (Tert) and Homeodomain-only protein X (Hopx), two markers of + 4 stem cells and the marker of noncanonical wnt pathway (wnt5, involved in inflammatory pathway) (Additional file 3: Fig. S3D) but At day 50, mice exposed to TiO 2 had an increased mRNA levels of colonic CD44, Leucine-rich repeatcontaining G-protein coupled receptor 5 (Lgr5), Achaete-scute complex homolog 2 (Ascl2) and Musashi RNA-binding protein 1 (Musashi), three markers of CBC, Telomerase reverse transcriptase (Tert) and Homeodomain-only protein X (Hopx), two markers of + 4 stem cells and the marker of noncanonical wnt pathway (wnt5, involved in inflammatory pathway) (Additional file 4: Fig. S4D) but We observed a significant reduction of organoid growth at day 9 postorganoid culture obtained from TiO 2 -exposed mice compared to control at day 30 (Fig. 3E) but the survival of colonic organoids was similar between both TiO 2 -treated and untreated group (Fig. 3F) We observed a significant reduction of organoid growth at day 9 postorganoid culture obtained from TiO 2 -exposed mice compared to control at day 30 (Fig. 3F) but the survival of colonic organoids was similar between both TiO 2 -treated and untreated group (Fig. 3E) Finally, since oxidative stress and/or DNA meth-ylation are well known to regulate gene expression, we monitored the impact of exposure to TiO 2 on the oxida-tive balance as well as DNA methylation of the colonic epithelium (Fig. 3G, H; Additional file 4: Fig. S4H) Finally, since oxidative stress and/or DNA meth-ylation are well known to regulate gene expression, we monitored the impact of exposure to TiO 2 on the oxida-tive balance as well as DNA methylation of the colonic epithelium (Fig. 3G, H; Additional file 4: Fig. S4G)

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Six weeks after microbiota transfer, permeability and mRNA levels of Occludin, Tpj1, Tpj2 and Mylk as well as Il1b, Il12, Tnfa and Ifng were assessed (Fig. 5B, C).As Six weeks after microbiota transfer, permeability and mRNA levels of Occludin, Tpj1, Tpj2 and Mylk as well as Il1b, Il12, Tnfa and Ifng were assessed (Fig. 5B-D).As As illustrated in Fig. 5B, the transfer of T iO 2 -triggered microbiota dysbiosis to healthy germfree mice led to significantly increased paracellular intestinal permeability (Fig. 5B), increased mRNA level of Mylk, and reduced mRNA level of Tjp1 and Tjp2 (Fig. 5C) As illustrated in Fig. 5B, the transfer of T iO 2 -triggered microbiota dysbiosis to healthy germfree mice led to significantly increased paracellular intestinal permeability (Fig. 5B), increased mRNA level of Mylk, and reduced mRNA level of Tjp1 and Tjp2 (Fig. 5C) in offspring at day 30 We observed that alteration of homeostasis of the colonic mucosa related to early life exposure to TiO 2 O 2 did not persist until adult 17 weeks of age as monitored for permeability, cytokine and other inflammatory markers i. e. in the group unchallenged for DSS mice exposed to TiO 2 superpose with mice unexposed (Fig. 6; Additional file 7: Fig. S7A) We observed that alteration of homeostasis of the colonic mucosa related to early life exposure to TiO 2 did not persist until adult 17 weeks of age as monitored for permeability, cytokine and other inflammatory markers i. e. in the group unchallenged for DSS mice exposed to TiO 2 superpose with mice unexposed (Fig. 6; Additional file 7: Fig. S7) However, as illustrated in Fig. 6B-H, perinatal exposure to TiO 2 enhanced significantly the loss of body weight and the DAI induced by DSS However, as illustrated in Fig. 6B-G Perinatal exposure to TiO 2 also exacerbated the colitis, as evidenced by a reduced colon length associated with increased colonic mRNA expression and protein levels of IL-1β, IL-4, IL-12, IL-13, IFNγ and TNF-α (Additional file 6: Fig. S6A and additional File 7: FigS7E) Perinatal exposure to TiO 2 also exacerbated the colitis, as evidenced by a reduced colon length associated with increased colonic mRNA expression and protein levels of IL-1β, IL-4, IL-12, IL-13, IFNγ and TNF-α (Additional file 7: Fig. S7)

Section Originally published text Corrected text
Perinatal exposure to TiO 2 also aggravated significantly the alterations of intestinal permeability, as evidenced by an increased Dextran-FITC flux, mRNA expression of MLCK and a reduced mRNA level of Tjp1 (Fig. 6G) Perinatal exposure to TiO 2 also aggravated significantly the alterations of intestinal permeability, as evidenced by an increased 4 kDa Dextran-FITC flux, mRNA expression of MLCK and a reduced mRNA level of Tjp1 (Fig. 6G) In contrast, at the 17th week of life, there was no longer any significant difference in terms of permeability, cytokine or other inflammatory markers i. e. in the group unchallenged for DSS mice exposed to TiO 2 superpose with mice unex-posed (Fig. 7D-H) In contrast, at the 17th week of life, there was no longer any significant difference in terms of permeability, cytokine or other inflammatory markers i. e. in the group unchallenged for DSS mice exposed to TiO 2 superpose with mice unex-posed (Fig. 7E-G) The colitis was exacerbated in these animals, as evidenced by a reduced colon length associated with increased colonic mRNA expression and protein levels of IL-1β, IL-4, IL-12, IL-13, IFNγ and TNF-α (Additional file 8: Fig. S8 A and Additional file 7: Fig. S7E) The colitis was exacerbated in these animals, as evidenced by a reduced colon length associated with increased colonic mRNA expression and protein levels of IL-1β, IL-4, IL-12, IL-13, IFNγ and TNF-α (Additional file 8: Fig. S8 and file 7: Fig. 7E) Organoid stem cell survival (number of organoids formed), and growth capacity (organoid area (µm 2 )) were followed three, six, nine and twelve days after plating with a wide field transmission microscope (Apotome Zeiss, 10X lens) Organoid stem cell survival (number of organoids formed), and growth capacity (organoid area (µm 2 )) were followed three, six and nine days after plating with a wide field transmission microscope (Apotome Zeiss, 10X lens)

Figure 3 Figure 3
Figure 3 Impact of perinatal exposure to foodborne TiO 2 on colonic epithelium at day 30.A-D Wild type female mice have been exposed to TiO 2 (9 mg/ BW/Day) Figure 3 Impact of perinatal exposure to foodborne TiO 2 on colonic epithelium at day 30.A-D Wild type female mice have been exposed to TiO 2 (9 mg/Kg of BW/Day)