Abstract
Bacteriocins are toxins produced by bacteria to kill competitors of the same species. Theory and laboratory experiments suggest that bacteriocin production and immunity play a key role in the competitive dynamics of bacterial strains. The extent to which this is the case in natural populations,especially human pathogens, remains to be tested. We examined the role of bacteriocins in competition using Pseudomonas aeruginosa strains infecting lungs of humans with cystic fibrosis (CF). We assessed the ability of different strains to kill each other using phenotypic assays, and sequenced their genomes to determine what bacteriocins (pyocins) they carry. We found that(i) isolates from later infection stages inhibited earlier infecting strains less,but were more inhibited by pyocins produced by earlier infecting strains and carried fewer pyocin types; (ii) this difference between early and late infections appears to be caused by a difference in pyocin diversity between competing genotypes and not by loss of pyocin genes within a lineage overtime; (iii) pyocin inhibition does not explain why certain strains outcompete others within lung infections; (iv) strains frequently carry the pyocin-killing gene, but not the immunity gene, suggesting resistance occurs via other unknown mechanisms. Our results show that, in contrast to patterns observed in experimental studies, pyocin production does not appear to have a major influence on strain competition during CF lung infections.
Highlights
Bacteria produce antimicrobial toxins, termed bacteriocins, to kill competitors [1]
In P. aeruginosa infections of the cystic fibrosis (CF) lung: (i) isolates from later infection stages caused less inhibition of other strains, were significantly more inhibited by the pyocins produced by other strains and carried a significantly lower diversity of pyocin types; (ii) pyocin genes were not lost from a chronic transmissible strain over time; (iii) within infections, over time, there is no change in inhibition/inhibiting levels or pyocin diversity; (iv) pyocin inhibition profiles do not significantly explain which strains persist longer within lung infections; (v) 35% of S pyocins occurred only as the killing gene, without the percentage of strains resistant (%)
We found no support for the hypothesis that certain strains are able to achieve dominance in the CF lung through bacteriocins
Summary
Bacteria produce antimicrobial toxins, termed bacteriocins, to kill competitors [1]. A number of experimental studies have shown that bacteriocins can play a key role in competitive dynamics among closely related bacterial strains [2,3]. Bacteriocin ‘producers’ can invade and outcompete ‘sensitive’ strains that are killed by that toxin. P. aeruginosa one strain usually carries and releases multiple types of bacteriocins known as pyocins, which have a diversity of killing and resistance mechanisms in addition to the toxin– antitoxin systems [2,7]. We examined the extent to which different strains where able to produce pyocins that inhibited the growth of other strains, comparing: (i) isolates sampled from non-lung environments and 13 CF Danish patients at different stages of infection and (ii) isolates sampled from a longitudinal study following the infection dynamics of strains within eight CF Danish patients. While it has been observed that some strains appear to not be killed by S pyocins, despite lacking the immunity gene for that pyocin, the relative occurrence and importance of this in nature remains unknown [24]
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