S in thefundus of mice infected with both species (Fig. 7C). The expression of Tff2 was drastically improved at 52 weeks postinfection in the fundus (fold transform for ASB1.four, six.49 three.32, and for SS1, three.44 1.49) (see Fig. S3 within the supplemental material). Muc4,iai.asm.orgInfection and ImmunityMuc13 and SPEM Induced by H. heilmannii Sensu StrictoFIG six Analysis of parietal cells inside the fundus with the PAC1-R Proteins Storage & Stability stomach of Helicobacter-infected and manage mice. (A to C) Expression levels of Atp4a (A), Atp4b (B), andKcnq1 (C) in the fundus with the stomach of H. heilmannii ASB1.4- and H. pylori SS1-infected mice are shown. Data are presented as fold modifications in gene expression normalized to three reference genes and relative to the final results for the negative-control group, which are set as 1. Substantial variations in expression levels amongst the infected groups along with the negative-control group at a particular time point (ANOVA) are indicated (, P 0.05; , P 0.001). (D to F) Immunohistochemical staining for the hydrogen potassium ATPase. (D) ATPase staining of your fundus of a ROR2 Proteins Recombinant Proteins sham-inoculated mouse. (E and F) Loss of parietal cells (arrows) was observed in the fundus with the stomach of a mouse infected with H. heilmannii ASB1.4 for 52 weeks (bar 30 m). (G) The mean numbers of parietal cells in the fundus in the stomach from mice infected with Helicobacter for 52 weeks and manage mice are shown. The amount of parietal cells in each stomach was determined by counting ATPase-positive cells in 5 randomly chosen high-power fields in the degree of the gastric pits. Significant differences amongst Helicobacter-infected and control animals (ANOVA) are indicated (, P 0.001).August 2014 Volume 82 Numberiai.asm.orgLiu et al.FIG 7 Determination of mucous metaplasia within the fundus in the stomach of Helicobacter-infected mice. (A to C) mRNA expression levels of Muc4 (A), Dmbt1 (B), and pIgR (C) in the fundus with the stomach of H. heilmannii ASB1.4- and H. pylori SS1-infected mice are shown. Information are presented as fold alterations in gene expression normalized to three reference genes and relative to the final results for the negative-control group, that are set as 1. Information are shown as indicates normal deviations. Considerable variations in expression level involving the infected groups plus the negative-control group at a specific time point (ANOVA) are indicated (, P 0.05; , P 0.001). (D) PAS-Alcian blue staining from the forestomach/stomach transition zone of a sham-inoculated mouse (bar 30 m). (E and F) PAS-Alcian blue staining on the antrum (E) as well as the fundus (F) of the stomach of a mouse infected with H. heilmannii ASB1 for 24 weeks (bars ten m). (G) PAS-Alcian blue staining with the forestomach/stomach transition zone of a mouse infected with H. heilmannii ASB1 for 52 weeks (bar 30 m). (E to G) Metaplastic columnar cells, mainly initiating in the transition zone junction involving the forestomach and glandular epithelium along the lesser curvature (G) and, to a lesser extent, in the antrum (E) and fundus (F) from the stomach of Helicobacter-infected mice are indicated in blue. (H) The imply numbers ofiai.asm.orgInfection and ImmunityMuc13 and SPEM Induced by H. heilmannii Sensu StrictoDmbt1, pIgR, and Tff2 have already been described to become associated to SPEM with chronic inflammation (6, 26). PAS-Alcian blue staining at 34 and 52 weeks postinfection showed evidence for mucous metaplasia, with metaplastic columnar glands primarily initiating in the transition zone junction among the forestomach and glandular epitheliu.