The Pseudomonas aeruginosa 1244 pilin glycan enhances twitching motility and pathogenesis in vitro.

Pseudomonas aeruginosa is drug-resistant pathogen that is commonly acquired during hospital stays. This bacterium produces type IV pili which are adhesins and motor appendages that mediate a surface motility referred to as “twitching.” These pili are polymers of protein subunits referred to as pilin. The pilin subunit of P. aeruginosa 1244 is glycosylated. Previous studies have shown that the pilin glycan affects the efficiency of twitching motility under certain conditions and the surface polarity of these fibers. We tested whether glass surfaces, EDTA, spermine, or CTAB affected twitching motility. Interestingly, the isogenic mutant strain lacking the pilin glycan (1244G7) showed decreased twitching compared to wild type bacteria. From a previous experiment, we found that Human Beta Defensin 2 (HBD2) inhibited the growth of the wild type bacteria but did not diminish the growth of 1244G7. Therefore, we hypothesized that HBD2 would diminish the pathogenesis of P. aeruginosa 1244 during an in vitro infection. To test this, human embryonic kidney cells (HEK-293) were infected with P. aeruginosa 1244 or 1244G7 bacteria. Surprisingly, HBD2 did not increase the viability of the host cells infected with P. aeruginosa 1244. However, wild-type P. aeruginosa 1244 bacteria exhibited increased toxicity compared to the 1244G7 strain suggesting that the pilin glycan is important in pathogenesis.