Probiotic yeast Saccharomyces
boulardii exerts
direct probiotic action on pathogenic E. coli by
trapping them on surfaces and inactivating toxic lipopolysaccharides.
Using optical dark-field microscopy, we show that nonpathogenic E. coli cells also readily bind probiotic S. boulardii. More importantly, the adhered nonpathogenic E. coli progressively damage S. boulardii cell walls and
lyse them. Co-cultured methylene blue-supplemented agar-plate assay
indicates that rough lipopolysaccharides might be playing a key role
in S. boulardii cell wall damage. When experiments
are repeated with lipopolysaccharide-depleted E. coli and also lipopolysaccharide-deficient E. coli,
adhesion decreases substantially. The co-cultured assay further reveals
that free lipopolysaccharides, released from E. coli, are also causing damage to S. boulardii walls
like adhered E. coli. These new findings contradict
the known S. boulardii–E. coli interaction mechanisms. We confirm that E. coli cells do not bind or damage human erythrocyte cell walls; therefore,
they have not developed pathogenicity. The combined results demonstrate
the first example of nonpathogenic E. coli being
harmful to probiotic yeast S. boulardii. This finding
is important because gut microbial flora contain large numbers of
nonpathogenic E. coli. If they bind or damage probiotic S. boulardii cell walls, then the probiotic efficiency toward
pathogenic E. coli will be compromised.