Lipid profiles of Helicobacter pylori colony variants.
A phase variation in Helicobacter pylori has been previously described. In one phase the bacterium had a cell wall lipid content typical for gram-negative bacteria (HpL), whereas in the other phase the bacterium was found to have a cell wall with increased amounts of lysophospholipids (HpS). The conversion is spontaneous, but could also be induced by acid (HpS(ind)) and was associated with in vitro release of Vac A and urease. The purpose of the present study was to determine the full phospholipid content of the cell wall to indicate a molecular mechanism of the colony variation. There were no appreciable differences between the lipid profiles of HpS and HpS(ind), while there were major differences between HpL and the S-variant. In the S-variant, lysophospholipids constituted about 50% of the total phospholipids, as compared to less than 2% in the L-variant. The proportion of total and individual cholesteryl glucosides also showed considerable changes. HpL was dominated by the phosphate-linked cholesteryl glucoside (72%) while the acylated cholesteryl glucoside was the main cholesteryl glucoside of the S-variant (65%). Our results demonstrate a dramatic change in cell wall properties after acid induction and spontaneously in vitro, and suggest some molecular mechanisms for this variation from an in vitro non-virulent to a virulent variant.
Institute of Microbiology, National Hospital, Oslo, Norway.
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Tannaes
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Bukholm
D002308:Cardiolipins / Q000032:analysis; D002473:Cell Wall / Q000737:chemistry; D002784:Cholesterol / Q000032:analysis; D005227:Fatty Acids / Q000032:analysis; D016480:Helicobacter pylori / Q000737:chemistry*; D008055:Lipids / Q000032:analysis*; D010743:Phospholipids / Q000032:analysis
D002308:Cardiolipins; D005227:Fatty Acids; D008055:Lipids; D010743:Phospholipids; D002784:Cholesterol