Probiotic yeast <i>Saccharomyces
boulardii</i> exerts
direct probiotic action on pathogenic <i>E. coli</i> by
trapping them on surfaces and inactivating toxic lipopolysaccharides.
Using optical dark-field microscopy, we show that nonpathogenic <i>E. coli</i> cells also readily bind probiotic <i>S. boulardii.</i> More importantly, the adhered nonpathogenic <i>E. coli</i> progressively damage <i>S. boulardii</i> cell walls and
lyse them. Co-cultured methylene blue-supplemented agar-plate assay
indicates that rough lipopolysaccharides might be playing a key role
in <i>S. boulardii</i> cell wall damage. When experiments
are repeated with lipopolysaccharide-depleted <i>E. coli</i> and also lipopolysaccharide-deficient <i>E. coli</i>,
adhesion decreases substantially. The co-cultured assay further reveals
that free lipopolysaccharides, released from <i>E. coli</i>, are also causing damage to <i>S. boulardii</i> walls
like adhered <i>E. coli</i>. These new findings contradict
the known <i>S. boulardii</i>–<i>E. coli</i> interaction mechanisms. We confirm that <i>E. coli</i> 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 <i>E. coli</i> being
harmful to probiotic yeast <i>S. boulardii</i>. This finding
is important because gut microbial flora contain large numbers of
nonpathogenic <i>E. coli</i>. If they bind or damage probiotic <i>S. boulardii</i> cell walls, then the probiotic efficiency toward
pathogenic <i>E. coli</i> will be compromised.