| Summary: | <p>Abstract</p> <p>Background</p> <p>Studies with the nematode model <it>Caenorhabditis elegans</it> have identified conserved biochemical pathways that act to modulate life span. Life span can also be influenced by the composition of the intestinal microbiome, and <it>C</it>. <it>elegans</it> life span can be dramatically influenced by its diet of <it>Escherichia coli</it>. Although <it>C</it>. <it>elegans</it> is typically fed the standard OP50 strain of <it>E</it>. <it>coli</it>, nematodes fed <it>E</it>. <it>coli</it> strains rendered respiratory deficient, either due to a lack coenzyme Q or the absence of ATP synthase, show significant life span extension. Here we explore the mechanisms accounting for the enhanced nematode life span in response to these diets.</p> <p>Results</p> <p>The intestinal load of <it>E</it>. <it>coli</it> was monitored by determination of worm-associated colony forming units (cfu/worm or coliform counts) as a function of age. The presence of GFP-expressing <it>E</it>. <it>coli</it> in the worm intestine was also monitored by fluorescence microscopy. Worms fed the standard OP50 <it>E</it>. <it>coli</it> strain have high cfu and GFP-labeled bacteria in their guts at the L4 larval stage, and show saturated coliform counts by day five of adulthood. In contrast, nematodes fed diets of respiratory deficient <it>E</it>. <it>coli</it> lacking coenzyme Q lived significantly longer and failed to accumulate bacteria within the lumen at early ages. Animals fed bacteria deficient in complex V showed intermediate coliform numbers and were not quite as long-lived. The results indicate that respiratory deficient Q-less <it>E</it>. <it>coli</it> are effectively degraded in the early adult worm, either at the pharynx or within the intestine, and do not accumulate in the intestinal tract until day ten of adulthood.</p> <p>Conclusions</p> <p>The findings of this study suggest that the nematodes fed the respiratory deficient <it>E</it>. <it>coli</it> diet live longer because the delay in bacterial colonization of the gut subjects the worms to less stress compared to worms fed the OP50 <it>E</it>. <it>coli</it> diet. This work suggests that bacterial respiration can act as a virulence factor, influencing the ability of bacteria to colonize and subsequently harm the animal host. Respiratory deficient bacteria may pose a useful model for probing probiotic relationships within the gut microbiome in higher organisms.</p>
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