Fig. 1: ADM is increased in gastric mucosa of H. pylori-infected patients and mice. | Cell Death & Disease

Fig. 1: ADM is increased in gastric mucosa of H. pylori-infected patients and mice.

From: Helicobacter pylori-induced adrenomedullin modulates IFN-γ-producing T-cell responses and contributes to gastritis

Fig. 1

a ADM mRNA expression in gastric mucosa of uninfected donors (n = 40) and H. pylori-infected patients (n = 70) was compared. b The correlation between ADM expression and H. pylori colonization in gastric mucosa of cagA+ H. pylori-infected patients was analyzed. c ADM mRNA expression in gastric mucosa of uninfected donors (n = 40), cagA− H. pylori-infected (n = 24), and cagA+ H. pylori-infected (n = 46) patients was compared. d Dynamic changes of ADM mRNA expression in WT H. pylori-infected, ΔcagA-infected, and uninfected mice. n = 5 per group per time point in d. e ADM protein in gastric mucosa of uninfected donors, cagA− H. pylori-infected, and cagA+ H. pylori-infected patients, or in gastric mucosa of WT H. pylori-infected, ΔcagA-infected, and uninfected mice on day 21 p.i., was analyzed by immunohistochemical staining. Scale bars: 100 µ. f ADM protein in gastric mucosa of uninfected donors, cagA– H. pylori-infected, and cagA+ H. pylori-infected patients was analyzed by western blot and statistically analyzed (n = 3). g ADM mRNA expression and ADM protein in human primary gastric mucosa from uninfected donors infected with WT H. pylori or ΔcagA ex vivo, analyzed by real-time PCR and western blot and statistically analyzed (n = 3). The results are representative of three independent experiments. The horizontal bars in panels a and c represent mean values. Each ring or dot in panels a–c represents one patient or donor. *P < 0.05, and **P < 0.01 for groups connected by horizontal lines compared, or compared with uninfected mice.

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