Abstract
Lipopolysaccharide from the gastroduodenal pathogen Helicobacter pylori was tested for its ability to induce mitogenicity in mouse spleen cells, pyrogenicity in rabbits, and toxic lethality in galactosamine-sensitized mice. Compared with those for enterobacterial lipopolysaccharide, mitogenicity and pyrogenicity were a thousand-fold lower and lethal toxicity was 500-fold lower. We suggest that the phosphorylation pattern and acylation in lipid A are responsible for the low biological activity.