A, Cellular inflammation in the gastric mucosa of Helicobacter pylori infected gerbils. Mononuclear cell (MNC) and polymorphonuclear cell (PMN) infiltration scores were graded from 0 (absent/normal) to 5 (maximal intensity) in corpus and antrum Mongolian gerbil tissue, presented as means ± standard errors. *P <.05; **P <.01 compared with 1 month. Both MNC and PMN infiltration peaked significantly 6 months after infection in antrum Mongolian gastric mucosa. B, Loss of blood group antigen–binding adhesin (BabA) expression during infection. An mean of 7 H. pylori colonies (range, 2–20 colonies) were picked from each gerbil as output strains, and the BabA expression levels of each output strain recovered from gerbils were measured by immunoblot analysis. The levels are presented as fold-induction of BabA expression, compared with input strain TN2GF4. BabA expression increased after 1 month after infection and diminished thereafter. Immunoblot results, representing BabA-expression level in the input strain and in the different output strains, are also shown. C, Leb-receptor binding activity in clones recovered after infection. Binding to the ¹²⁵I-Leb conjugate was measured for 27 selected output clones (10 randomly selected BabA expressing clones, 14 randomly selected BabA nonexpressing clones, and all 3 BabA weak-expressing clones) and for the input strain TN2GF4 and 10 randomly selected single clones of the input strain TN2GF4 with radioimmunoassay. Binding activity is given as (%) of bound ¹²⁵I-Leb.

A and B show Leb- and H1-receptor binding properties of strain TN2GF4. A, One representative set of 3 independent radioimmunoassay measurements of Leb- and H1-binding activity are presented as percentage bound glycoconjugate for strains TN2GF4 (input), 17875/Leb, and 17875/sLex (negative control). B, Receptor-binding affinity conjugate was measured according to Scatchard. The slope of the curve represents the H1 receptor-binding affinity. C, Adherence of output TN2GF4 to Mongolian gerbil gastric mucosa. Tissue sections of Mongolian gerbils gastric mucosa 1 month after infection were incubated with: (a) α-H1 monoclonal antibody and fluorochrome Alexa 488 for detection of H1 expression; (b) co-localization of FITC-labelled bacteria cells of a 1-month output TN2GF4 (BabA+) clone isolated from the corresponding gerbil and H1 expression; (c) FITC-labelled bacteria cells of a 1-month output TN2GF4 (BabA+) clone isolated from the corresponding gerbil; (d) FITC-labelled bacterial cells of the 1-month output TN2GF4 clone that were pre-incubated with H1 prior to incubation with the tissue sections or FITC-labelled bacterial cells of strain 17875/Leb; (e) FITC-labelled bacterial cells of strains 17875/Leb; (f) FITC-labelled bacterial cells of strains 17875/Leb that were pre-incubated with H1 prior to incubation with the tissue sections.

Cellular inflammation and mucosal thickness in gastric mucosa of gerbils re-inoculated with recovered Helicobacter pylori 3 months after infection. Polymorphonuclear cell (PMN), mononuclear cell (MNC), and H. pylori density scores were graded from 0 (absent/normal) to 5 (maximal intensity) in corpus and antrum Mongolian gerbil tissue 3 months after inoculation. Mucosal thickness was measured in millimeters. Data are presented as mean values ± standard errors. *P <.05; **P <.01.

Histological findings for uninfected control gerbils and gerbils at 3 months after infection. A, D, G, J, and M correspond to antrum gerbil mucosa; B, E, H, K, and N correspond to the transitional zone (mucoparietal glands); and C, F, I, L, and O correspond to the corpus mucosa. The morphology is presented by hematoxylin and eosin staining of uninfected (A–C) and infected (G–I) gerbil gastric tissue. The corresponding regions were immunostained with monoclonal H1 antibodies and detected with a brown chromogen. D–F represent unifected gerbils and J–L represent Helicobacter pylori infected mucosa. Expression of H1 antigen was found in D–F (ie, uninfected mucosa). No staining or faint staining of H1 was seen in J–L (ie, H. pylori–infected mucosa). H. pylori bacteria cells were detected with α–H. pylori polyclonal antibody and stained brown (M–O). Enlargement of areas with H. pylori staining are inserted in figures M–O. Scale bars represent 50 μm.

Expression of sialyl-Lewis x (sLex) antigen in inflamed gerbil gastric mucosa and Helicobacter pylori adherence. sLex expression in gerbil mucosa was probed with either sLex monoclonal antibody or with the SabA-expressing H. pylori strain 17875/sLex. A, Uninfected gerbil gastric tissue overlaid with FITC-labelled 17875/sLex. B–E, Gerbil mucosa obtained at 1, 3, 6, and 18 months after inoculation and probed with strain 17875/sLex. F, Neuraminidase-treated gerbil tissue sections obtained at 1 month after infection and incubated with 17875/sLex. G, gerbil gastric mucosa obtained 1 month after infection and detected with monoclonal sLex antibodies and Alexa 568. H, Neuraminidase-treated gerbil tissue sections obtained 1 month after infection and incubated with sLex monoclonal antibodies and Alexa 568.