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Recent advances in our understanding of Helicobacter pylori-phagocyte interactions indicate that these organisms actively modulate phagocyte function in order to retard phagocytosis, while simultaneously inducing a strong respiratory burst. The central players in this dynamic include H. pylori neutrophil activating protein and factors that are associated with the cag pathogenicity island type IV secretion apparatus. Additionally, catalase, alkyl hydroperoxide reductase, and factors that are unique to type I strains allow bacteria to resist phagocytic killing.
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Lee‐Ann H. Allen (2001) studied this question.
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