Salivary MUC5B-mediated adherence (ex vivo) of Helicobacter pylori during acute stress

Objective: Biochemical host defenses at mucosal sites, such as the oral cavity, play a key role in the regulation of microbial ecology and the prevention of infectious disease. These biochemical factors have distinct features, some of which benefit the host and some that benefit bacteria. We investigated the effects of acute stress on the salivary levels of the carbohydrate structure sulfo-Lewis(a) (sulfo-Le(a)), which is linked to the mucosal glycoprotein MUC5B. Sulfo-Le(a) was recently identified as an adhesion molecule for Helicobacter pylori; therefore, we also measured saliva-mediated adherence (ex vivo) of H. pylori. The oral cavity is suspected to be involved in the transmission of H. pylori. Methods: Saliva was collected from 17 undergraduates before (baseline), during (stress), and after (recovery) exposure to a video showing surgical procedures. In addition, blood pressure, an impedance cardiogram, and an electrocardiogram were recorded. Results: During stressor exposure, participants reported increased state anxiety. In addition, stroke volume increased and heart rate decreased. The stressor induced a strong increase in salivary sulfo-Le(a) concentration (U/ml), sulfo-Le(a) output (U/min), sulfo-Le(a)/total protein ratio (U/mg protein), and saliva-mediated adherence lex vivo) of H. pylori. As expected, sulfu-Le(a) concentration correlated with the adherence of H. pylori (r = 0.72, p < .05). It was demonstrated that the observed adherence was induced by MUC5B and that the carbohydrate structure sulfo-Le(a) contributed to this process. Conclusions: Our study demonstrated a direct link between stress-mediated biochemical changes and altered host-microbe interactions in humans. Increased bacterial adherence may be a contributing factor in the observed relationship between stress and susceptibility to infectious disease.