Figure 6.

Lm translocates through IECs in an InlA-dependent but LLO- and ActA-independent manner. (A) Intestinal loops were infected with 109 of the indicated Listeria strains, and bacteria were quantified in the lamina propria after 30 min. n = 30 villi from three mice. (B) Intestinal loops were infected with the indicated Listeria strains, and bacteria were quantified in the spleen after 30 min of infection. n = 5 mice. (C) Quantification of Lm located in IECs in tissue treated with 10 µg/ml nocodazole, 10 µg/ml colchicine, or their corresponding vehicles (control) for 50 min out of 60 min of Lm infection. n = 11, 15, and 14 infected villi from three mice, respectively. (D) Optical sections of Lm-infected villus treated with PBS as a control, nocodazole, or colchicine for 50 min out of 60 min of Lm infection. Arrows points to Lm either inside epithelial cells or in the lamina propria. (E) Quantification of Lm located in intestinal epithelium or in the lamina propria of tissue treated with PBS (control), 20 µg/ml TAT-NSF700, or 20 µg/ml TAT-NSF scr for 30 min and during Lm infection for 45 min. n = 20 infected villi from three mice. (A–C and E) Error bars indicate SD. (F) Optical sections of intestinal villus treated with PBS as a control, TAT-NSF peptide, or TAT-NSF scr for 30 min and infected with Lm (arrows) in the presence of the peptides for 45 min. (D and F) Tissues are stained for F-actin. Pictures are representative of three mice. (G) TEM sections of PBS-, TAT-NSF700–, or TAT-NSF700scr–treated tissues. Pictures are representative of two mice. Bars: (D and F) 10 µm; (G) 2 µm.

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