New acquisitions in Helicobacter pylori characteristics

The protection of Helicobacter pylori from the gastric acid exerted by urea se is based on an increase of the bacterial periplasmic pH and membrane pot ential. ammonia generated from urea induces apoptosis of gastric cells in v itro, and inhibits gastric somatostatin release in animals, which could hav e consequences on the physiology of digestion in general. The type s1/m1 st ructure of the vacA gene is associated with the production of high levels o f cytotoxin. Strains with m2 region type, formerly considered devoid of tox ic activity, are fully toxic when assayed with cell lines other than HeLa c ells, which possibly lack receptors for m2 VacA type The enhanced gastric m ucosa damage associated with infection by cytotoxic organisms could be expl ained by the varying of effects exerted by VacA on target cells: extracellu lar secretion of acidic hydrolases, cytoskeletal alterations, actin rearran gement, reduction of epidermal growth factor binding to its receptor inhibi tion of the stimulation of CD4(+) T cells proliferation induced by the anti gen presenting cells. Organisms that possess the pathogenicity island cag ( cag(+)) induce an increased inflammation and transduction of signals to the host cells; however, they reduce the apoptosis of colonised cells. The res ults of an investigation on the possible influence of a variable cagA statu s on the extension of apoptosis have indicated that this kind of programmed death is disengaged from the possession of cagA by Helicobacter pylori org anisms colonising the same gastric al eas. It is likely that the whole path ogenic potential of cag+ organisms is far from being completely explored, a s suggested by the recent finding that the expression of a bacterial adhesi n (called BabA) involved in binding to the blood group antigen Lewis b is a ssociated with the presence of cag.