Figure 1.

Electronic cigarettes trigger inflammation in the murine distal colon and disrupt the integrity of the murine gut barrier

(A) Schematic displays the key aspects of the murine model of vaping used in this study. Mice were exposed to air (negative control), nicotine-free e-cig (e-cig alone; MOD brand), or nicotine-containing e-cig (e-cig + 6 mg/mL nicotine) for 1 week or 3 months.

(B) Hematoxylin-eosin staining of distal colons after 1 week (left) or 3 months (right) of exposure to e-cig. Asterisks, inflammatory infiltrates; arrowheads, epithelial erosions.

(C) Bar graphs display the relative levels of expression of genes in the colon (black dots, male mice; red dots, female mice) that encode proteins that regulate epithelial tight junctions. Data are displayed as mean ± SEM. Statistical significance was estimated using either one-way ANOVA with Tukey's test (black ∗) or Mann-Whitney's test (red ∗); ∗p<0.05, ∗∗p <0.01 and ∗∗∗p <0.001.

(D) Schematic displays the key aspects of ex vivo disease modeling to interrogate the impact of vaping on the murine colonic epithelial barrier.

(E) Bar graphs display the percent change in TEER. Data are displayed as mean ± SEM (n = 3–4 independent experiments). UN, normal media; Air, air-infused media.

(F and G) EDMs were treated as indicated, fixed and stained for occludin (green) and DAPI (blue, nuclei), and analyzed by confocal microscopy. Bar graphs in (F) display the percent increase in the tight junction (TJ) “bursts” (indicative of disrupted TJs). Data are displayed as mean ± SEM (n = 3 fields/condition; 40–50 tricellular TJs/field). Statistical significance was estimated using one-way ANOVA with Tukey's test; ∗∗p <0.01. Confocal microscopic images in (G) are representative of EDMs, either untreated (UN) or after 4 h of treatment with air or e-cig-infused media. Scale bar, 10 μm.