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. 1999 Dec;45(6):804–811. doi: 10.1136/gut.45.6.804

Relation between clinical presentation, Helicobacter pylori density, interleukin 1β and 8 production, and cagA status

Y Yamaoka 1, T Kodama 1, M Kita 1, J Imanishi 1, K Kashima 1, D Graham 1
PMCID: PMC1727763  PMID: 10562576

Abstract

BACKGROUND—It is not known whether cagA+ Helicobacter pylori in duodenal ulcer (DU) have enhanced virulence compared with non-DU cagA+ H pylori.
AIMS—To investigate the relation between presentation, H pylori density, interleukin 1β (IL-1β) and IL-8 production, and cagA status.
METHODS—Fifty DU and 50 gastritis patients with cagA+ H pylori and 11 with cagA− infections were studied. Bacterial density and cytokine production were assessed using the same biopsies. Cytokine production was also measured from supernatants of medium following coculture of H pylori with MKN-45 cells.
RESULTS—There was no relation between H pylori density and cagA status. There was a dose dependent relation between mucosal cytokine levels and density of cagA+ H pylori. H pylori density increased to a threshold, followed by a rapid increase in cytokines and then a plateau. IL-1β and IL-8 levels in the antrum were greater in DU than in gastritis; in the corpus the cytokine level/H pylori differed irrespective of similar H pylori densities. However, cytokine production was similar in vitro, independent of presentation or biopsy site, suggesting that host factors are critical determinants of the inflammatory response. Mucosal IL-8 and IL-1β levels were low with cagA− and cagA+, cagE− H pylori infections.
CONCLUSIONS—The increase in antral IL-1β and IL-8 production and inflammation in DU is related to increased numbers of bacteria and not to an increase in cytokine production per cagA+ isolate. There was no evidence of enhanced virulence of H pylori from DU compared with cagA+ non-DU H pylori.


Keywords: duodenal ulcer; Helicobacter pylori; interleukin 1β; interleukin 8; cagA

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Figure 1  .

Figure 1  

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Helicobacter pylori density in antrum and corpus. The end of the bars indicates the 25th and 75th percentiles. The 50th percentile (median) is indicated with a solid line in the box; the broken line indicates mean value. The 10th and 90th percentiles are indicated with error bars. DU, duodenal ulcer.

Figure 2  .

Figure 2  

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Relation between Helicobacter pylori density by culture and cellular infiltration in cagA+ cases. DU, duodenal ulcer; MNC, mononuclear cell; PMN, polymorphonuclear cell.

Figure 3  .

Figure 3  

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Mucosal interleukin (IL) 8 production. The end of the bars indicates the 25th and 75th percentiles. The 50th percentile (median) is indicated with a line in the box and the 10th and 90th percentiles are indicated with error bars. *Two cagA+ gastritis cases with extremely low in vitro IL-8 production, which indicate cagA positive, cagE, cagG negative strains. DU, duodenal ulcer.

Figure 4  .

Figure 4  

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Relation between mucosal interleukin (IL) 1β and IL-8 production and Helicobacter pylori density of cagA+ strains in the antrum.

Figure 5  .

Figure 5  

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Relation between mucosal interleukin (IL) 1β and IL-8 production and Helicobacter pylori density of cagA+ strains in the corpus.

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