Gut 1999;45:804-811 ( December )

Article

Relation between clinical presentation, Helicobacter pylori density, interleukin 1 and 8 production, and cagA status Y Yamaoka^a, T Kodama^b, M Kita^c, J Imanishi^c, K Kashima^b, D Y Graham^a

^a Department of Medicine, Veterans Affairs Medical Centre and Baylor College of Medicine, Houston, Texas, USA, ^b Third Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan, ^c Department of Microbiology, Kyoto Prefectural University of Medicine, Kyoto, Japan

Correspondence to: Dr Y Yamaoka, Rm 3A320, Veterans Affairs Medical Centre (111D), 2002 Holcombe Blvd, Houston, TX 77030, USA.

Accepted for publication 23 June 1999

BACKGROUNDIt is not known whether cagA+ Helicobacter pylori in duodenal ulcer (DU) have enhanced virulence compared with non-DU cagA+ H pylori.
AIMSTo investigate the relation between presentation, H pylori density, interleukin 1 (IL-1) and IL-8 production, and cagA status.
METHODSFifty 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.
RESULTSThere 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-1 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-1 levels were low with cagA and cagA+, cagE H pylori infections.
CONCLUSIONSThe increase in antral IL-1 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 1; interleukin 8; cagA

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© 1999 by Gut
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