The transcriptional organization and heat inducibility of the major heat shock genes hrcA, dnaK, dnaJ, groEL, and htpG were analyzed on the transcriptional level in Helicobacter pylori strain 69A. The strongly heat-induced dnaK operon was found to be tricistronic, consisting of the genes hrcA, grpE, and dnaK. The dnaJ gene specified one monocistronic mRNA which was also heat inducible. The genes groES and groEL were transcribed as one strongly heat-inducible bicistronic mRNA which exhibited exactly the same induction kinetic as the dnaK operon. Surprisingly, transcription of the monocistronic htpG gene was switched off after heat shock. The data presented are discussed with regard to the different mechanisms regulating expression of heat shock genes in H. pyloriHelicobacter pylori is a gram-negative, spiral-shaped pathogenic bacterium that specifically colonizes the gastric epithelium of primates and is the causative agent of chronic, active type B gastritis in humans (3). The following genetic determinants contribute to the successful colonization of the gastric mucosa: a urease neutralizing the bacterial microenvironment by producing ammonia from the urea present in mucosal sections (9, 10, 14); motility in the gastric mucus and adhesion to the mucosal cell membrane, enabling H. pylori to avoid the extremely low pH of the gastric lumen (11,24,35); and the low-pH-induced synthesis of H. pylori gene products inhibiting acid secretion by mucosal cells (26). As has been demonstrated for all other bacterial species examined so far, H. pylori elicits a heat shock response. Thermoregulation plays an important role in virulence gene expression in pathogenic bacteria including Escherichia coli, Salmonella spp., Shigella spp., and Yersinia spp. Given the importance of the heat shock response in the pathogenesis of other enteric pathogens, this stress response may also play an important role in pathogenesis of H. pylorimediated gastritis.The major heat shock proteins GroES/GroEL and DnaK have been identified in H. pylori. The amount of GroEL increases after heat shock and acid shock (22,45). It has been proposed that GroEL may participate in protection and activity regulation of urease (12,36). An increase in the amount of DnaK after acid shock has also been observed (22). Furthermore, DnaK was reported to be involved in the modulation of glycolipid binding specificity of H. pylori at low pH (21).The aim of this study was to analyze expression of the major H. pylori heat shock genes at the transcriptional level under unstressed conditions and after heat shock. The availability of the published complete H. pylori genome sequence (38) made it possible to generate highly sensitive RNA probes allowing the detection of mRNA specified by the classical heat shock genes hrcA, dnaK, dnaJ, groEL, and htpG.Recently, Spohn and Scarlato demonstrated the negative regulation of the promoters preceding the dnaK and groE operons by the HspR/HAIR (HspR-associated inverted repeat) repressor/operator system in H. pylori G27 (34). Surprising...

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