A new article describes how H. pylori rapidly identifies and colonizes sites of minor injuries in the stomach, almost immediately interferes with healing at those injury sites, and so promotes sustained gastric damage.
Smoking, alcohol, excessive salt intake, and non-steroidal anti-inflammatory drugs cause damage to the tissue lining the stomach, and are associated with stomach ulcers. Scientists asked whether H. pylori can sense and respond to such damage and so contribute to disease development.
The researchers induced small stomach lesions in mice and observed that H. pylori bacteria can rapidly detect the injury site and navigate toward it. Within minutes, accumulation of bacteria interferes with repair of the tissue damage.
To examine how the bacteria accomplish this, the researchers also studied mice with larger stomach lesions (ulcers) that were subsequently infected with H. pylori. They found that H. pylori preferentially colonizes stomach tissue at injured ulcer sites, and there impairs healing of the damaged tissue. Selective colonization requires both bacterial motility and chemotaxis (the ability to change direction of movement in response to environmental cues), and higher levels of bacterial accumulation cause slower healing. However, when extremely high levels of immotile or chemotaxis-deficient bacteria are added to damaged tissue, they can also slow healing.
While the signals that attract H. pylori (but not benign stomach bacteria) toward injured tissue are not yet known, the researchers hope that their ability to rapidly measure H. pylori accumulation at the injured site now provides an experimental set-up to determine the factor(s) involved.