A neutrophil chemotactic factor present inH. pylori but absent inH. mustelae

Abstract

This study was designed to compare the capabilities of Helicobacter pylori and Helicobacter mustelae to generate neutrophil chemotactic activity (NCA) in vitro. H. pylori and H. mustelae were grown in parallel cultures under identical conditions. The cultures were washed and transferred to saline solution for 3 hr to avoid detecting nonspecific chemotactic activity from culture media. Supernatants were subjected to size-exclusion HPLC. All peaks from HPLC were collected and assayed for NCA. Peaks having significant NCA were subjected to gel electrophoresis. H. pylori generated 85.9 +/- 1.7% NCA compared to only 41.6 +/- 2.5% for H. mustelae (P < 0.001). The HPLC peak containing the highest NCA from H. pylori revealed a band on gel electrophoresis at approximately 10.5 kDa. This band was not present on gels from H. mustelae. We conclude that H. pylori produces a neutrophil chemotactic factor lacking from H. mustelae. This offers an explanation for the histologic difference between gastritides caused by these organisms.

Diethyl Phthalate, a Chemotactic Factor Secreted by Helicobacter pylori

“…These observations led others to investigate factors produced by H. pylori that cause monocyte and neutrophil chemotaxis (19,(22)(23)(24)(25)(26)(27)(28)(29)(30)(31). Specific factors identified include: H. pylori sonicate proteins of [25][26][27][28][29][30][31][32][33][34][35]25), urease and urease fragments (26), leukotrienes (22), fMLP (5), an 8.5-kDa factor (28), a 10.5-kDa factor (29), a 30-kDa porin protein (31), and a low molecular weight factor that is not fMLP (27,30).…”

“…Specific factors identified include: H. pylori sonicate proteins of [25][26][27][28][29][30][31][32][33][34][35]25), urease and urease fragments (26), leukotrienes (22), fMLP (5), an 8.5-kDa factor (28), a 10.5-kDa factor (29), a 30-kDa porin protein (31), and a low molecular weight factor that is not fMLP (27,30).…”

Rebamipide, a novel antiulcer agent, attenuates Helicobacter pylori induced gastric mucosal cell injury associated with neutrophil derived oxidants.

“…Several studies have already shown that H pyloni itself exhibits chemotactic activity for neutrophils. [1][2][3][4][5] We have also reported that H pylori elicited neutrophils produce toxic oxidants, which subsequently injure cultured gastric mucosal cells, and that ammonia, which is derived from urea by H pyloni associated urease enhances the mucosal cytotoxicity, which may be regulated by monochloramine.6 7 Considering these mechanisms, the agents that can inhibit either neutrophil activation or ammonia production are proposed to be effective for Hpyloni induced gastric mucosal injury. Rebamipide had been reported to promote mucus synthesis,8 mucosal prostaglandin content, and rapid ulcer healing.9 Moreover, it has recently been reported to inhibit the production of oxygen derived free radicals from stimulated neutrophils.10 In this report, we have evaluated whether rebamipide may influence active oxidant production elicited by H pyloni activated neutrophils and urease activity, and whether it attenuates gastric mucosal cell damage associated with H pylor activated neutrophils in vitro.…”

A low molecular weight factor is a significant mediator of non-opsonic neutrophil activation by Helicobacter pylori

“…Evans et al reported possible additional HpNAP cross-reactive bands by Western blotting [22]. In contrast to other studies, there was no evidence of strong activity associated with the 61-kDa urease subunit [15] or unknown 25±35-kDa [16] and 10.5-kDa [17] proteins. Differences in the preparation of extracts may account for these ®ndings.…”

“…The H. pylori urease protein may display chemo-attractive activity [15], as have uncharacterised 25±35-kDa and 10.5-kDa proteins [16,17]. The same 25±35-kDa chemo-attractant protein described by Nielsen and Andersen (1992) was also shown to activate neutrophils [16].…”