Eosinophil infiltration and degranulation inHelicobacter pylori-associated chronic gastritis

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Abstract
Eosinophil granules contain cationic proteins, including the major basic protein, which are toxic to mammalian tissue. While eosinophils have been observed to comprise part of the inflammatory reaction in acuteHelicobacter pylori gastritis, the role of the eosinophil in the pathogenesis of chronic gastritis is unknown. We evaluated whether eosinophil infiltration and degranulation are associated with chronic gastritis andH. pylori infection. We studied eight patients with chronicH. pylori antral gastritis, three with chronic antral gastritis in the absence ofH. pylori, 11 healthy age-matched volunteers without antral gastritis, and eight patients withH. pylori-negative chronic specific gastritis (three Crohn's antral gastritis and five Ménétrier's disease). Serial sections were stained with hematoxylin and eosin, with Giemsa, and by a specific indirect immunofluorescence technique for eosinophil granule major basic protein. Specimens were graded independently by three observers and scores of 0–3 were given for eosinophil infiltration and degranulation (0=none to 3=confluent infiltration and/or degranulation). InH. pylori antral gastritis, significantly greater eosinophil infiltration and degranulation were found compared to the normal group, Ménétrier's disease, and chronicH. pylori-negative gastritis. There was no significant difference between gastric Crohn's disease andH. pylori gastritis. The severity of chronic gastritis was significantly correlated with the eosinophil score. Eosinophil degranulation did not appear to be greater at or near sites of bacterial colonization in theH. pylori gastritis specimens. The results suggest that eosinophil infiltration and degranulation may be associated withH. pylori gastritis. We postulate that the release of toxic cationic proteins from eosinophils contributes to the inflammatory changes present inH. pylori gastritis.