Skip to main content
. 2011 Oct;79(10):4186–4192. doi: 10.1128/IAI.05602-11

Table 1.

Female 129/Sv mice but not male 129/Sv mice develop Helicobacter pylori-induced atrophic gastritis

Expt and micea Length of infection (mo) Median grade of pathology (interquartile range)b
Cellular infiltration (0–6) Mucus metaplasia (0–3) Atrophy (0–3)
Expt 1
    Male 129/Sv 2 1 (0.5–1.0) 0 (0–0) 0 (0–0)
    Female 129/Sv 2 1 (1–2.5) 0 (0–0) 0 (0–0.5)
    Male Muc1−/− 2 0.5 (0–2) 0 (0–0) 0 (0–1)
    Female Muc1−/− 2 3 (2.5–4.0)* 0 (0–0) 2 (1–2.5)*
Expt 2
    Male 129/Sv 0 (uninfected) 0 (0–0) 0 (0–0) 0 (0–0)
    Female 129/Sv 0 (uninfected) 0 (0–0) 0 (0–0) 0 (0–0)
    Male 129/Sv 6 1 (1–2.5) 0 (0–0) 0.5 (0–1.5)
    Female 129/Sv 6 4 (4–4)* 0 (0–0) 3 (2.5–3.0)*
a

In experiment 1, male and female wild-type or Muc1−/− 129/Sv mice (n = 11) were infected with H. pylori for 2 months, and then gastric pathology was assessed histologically. Gastritis in all mice was observed only in the corpus. Only the H. pylori-infected female Muc1−/− mice developed atrophic gastritis. In experiment 2, male and female wild-type 129/Sv mice (n = 8) were infected with H. pylori for 6 months or left uninfected. While the infected female mice developed a severe atrophic gastritis, infected male mice developed only a very mild gastritis. This demonstrates that the gender effect on gastritis was not related to Muc1 expression but was common for 129/Sv mice.

b

*, significantly greater cellular infiltrate and atrophy than in all other groups (P < 0.04; Mann-Whitney U test).