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. 1998 Jun;42(6):772–778. doi: 10.1136/gut.42.6.772

cagA positive and negative Helicobacter pylori strains are simultaneously present in the stomach of most patients with non-ulcer dyspepsia: relevance to histological damage

N Figura 1, C Vindigni 1, A Covacci 1, L Presenti 1, D Burroni 1, R Vernillo 1, T Banducci 1, F Roviello 1, D Marrelli 1, M Biscontri 1, S Kristodhullu 1, C Gennari 1, D Vaira 1
PMCID: PMC1727148  PMID: 9691913

Abstract

Background/Aims—Infection with Helicobacter pylori strains harbouring the cagA gene (cagA+) is associated with an increased risk of developing peptic ulcer and gastric cancer. The aim of this study was to assess whether H pylori isolates with different cagA status were present in patients with non-ulcer dyspepsia, and whether a variable cagA status is relevant to histological gastric mucosal damage and glandular cell proliferation. 
Methods—Well separated H pylori colonies (between 2 and 25) from primary plates, per gastric area, for each of 19 patients with non-ulcer dyspepsia were examined for cagA by hybridisation. Western blotting was used to examine both representative colonies for CagA expression and the patients' sera for antibody response to CagA. Glandular gastric cell proliferation was assessed immunohistochemically. 
Results—Of the 747 colonies examined, 45.3% were cagA+. All colonies from four patients were cagA+, and all colonies from two patients were cagA−. In 13 patients (68%) both cagA+ and cagA− colonies were found. CagA expression of isolates corresponded to their cagA status. H pylori strains with different CagA molecular masses were present in three patients. Results based on all 19patients studied showed that the prevalence of cagA+ colonies in areas with mucosal atrophy associated or not with intestinal metaplasia (67.9%) was significantly higher than in normal mucosa (44.7%) and mucosa from patients with chronic gastritis (44.0%) (p< 0.001). High levels of cell proliferation were associated with histological atrophy with or without intestinal metaplasia, but not with the possession of cagA by organisms colonising the same mucosal sites. 
Conclusions—Most patients with non-ulcer dyspepsia are infected by both cagA+ and cagA−H pylori colonies. The cagA status of infecting organisms may play a role in the development of atrophy and intestinal metaplasia. 



Keywords: gastritis; Helicobacter pylori infection; cagA; mucosal atrophy; cell proliferation

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Figure 1 .

Figure 1

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Hybridisation with cagA probe of subcultures of different H pylori colonies from primary plates streaked with biopsy samples taken from two gastric areas from the same patient. All 16 colonies from the antrum and 18 of 21 from the corpus are cagA+ (six of 13 colonies from the fundus were cagA+; data not shown). The arrows indicate the cagA− colonies. 


Figure 2 .

Figure 2

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Western blots showing , in three cases (lanes 1-3, 4-6, and 7-9), the simultaneous presence of H pylori strains with different CagA molecular mass in different areas of single patients. The strain in lane 1 was cagA−. The strains in lanes 10 and 11 were two cagA+ H pylori strains of similar CagA molecular mass isolated from two different gastric areas of a patient. The numbers on the right are the molecular masses in kDa of H pylori strains CCUG 17874 and G39. 


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