Abstract
Helicobacter pylori establishes chronic human stomach infections characterized by persistent inflammation. Previous work had identified a high-inflammation H. pylori mutant lacking the chemoreceptor TlpA. To understand H. pylori inflammation control, Johnson et al. (e00322-22) compared colonization dynamics and host response between the tlpA mutant and the wild type. Both strains caused inflammation at the late, chronic-infection stages, but surprisingly this inflammation fluctuated temporally and was offset in period between the wild type and the tlpA mutant. tlpA mutants also showed high early-infection bacterial numbers. These results suggest that chronic inflammation is more dynamic than previously thought and may be influenced by colonization properties of early infection.
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