CIRCULATING ANTIBODIES TO THE 60-KD HEAT-SHOCK-PROTEIN (HSP) FAMILY IN PATIENTS WITH HELICOBACTER-PYLORI INFECTION

Whilst the mechanism by which Helicobacter pylori causes different gas troduodenal diseases is uncertain, strains producing the cytotoxin-ass ociated protein (CagA) have greater pathogenicity. Hsps are immunogeni c molecules induced by inflammatory mediators. The aim of this study w as to assess pathogenicity of hsp antibodies in H. pylori-infected pat ients. ELISA techniques were used to assay sera of H pylori-positive p atients with gastritis, gastric atrophy, duodenal or gastric ulcer, an d H. pylori-negative controls, for antibodies to CagA and to human, my cobacterial, and in 20 sera, H. pylori (hspB) 60-kD hsp. IgA antibodie s to mycobacterial hsp60 in atrophy patients were elevated compared wi th patients with gastritis (P < 0.05) and with H. pylori-negative cont rols (P < 0.0005). IgA antibodies to human hsp60 in gastric atrophy pa tients were elevated compared with H. pylori-negative controls (P<0.05 ). Patients with atrophy (P<0.0005) and gastritis (P<0.05) who were Ca gA-positive had raised titres of anti-mycobacterial hsp60 IgA antibodi es compared with controls. IgA antibody levels to hspB were positively correlated with those to mycobacterial hsp60 (mhsp60) (P<0.05) and hu man hsp60 (hhsp60) (P<0.005). IgA antibodies to hsp60 are associated w ith gastroduodenal disease, particularly gastric atrophy, in H pylori- infected patients. Increased humoral responses to hsp60 could either c ontribute to gastric atrophy or result from greater gastric mucosal da mage induced by CagA-positive strains of H. pylori.