Abstract
Twitching motility-mediated biofilm expansion occurs via coordinated, multi-cellular collective behaviour to allow bacteria to actively expand across surfaces. Type-IV pili (T4P) are cell-associated virulence factors which mediate twitching motility via rounds of extension, surface attachment and retraction. The Chp chemosensory system is thought to respond to environmental signals to regulate the biogenesis, assembly and twitching motility function of T4P. In other well characterised chemosensory systems, methyl-accepting chemotaxis proteins (MCPs) feed environmental signals through a CheW adapter protein to the histidine kinase CheA to modulate motility. The Pseudomonas aeruginosa Chp system has an MCP PilJ and two CheW adapter proteins, PilI and ChpC, that likely interact with the histidine kinase ChpA to feed environmental signals into the system. In the current study we show that ChpC is involved in the response to host-derived signals serum albumin, mucin and oligopeptides. We demonstrate that these signals stimulate an increase in twitching motility, as well as in levels of 3'-5'-cyclic adenosine monophosphate (cAMP) and surface-assembled T4P. Interestingly, our data shows that changes in cAMP and surface piliation levels are independent of ChpC but that the twitching motility response to these environmental signals requires ChpC. Furthermore, we show that protease activity is required for the twitching motility response of P. aeruginosa to environmental signals. Based upon our data we propose a model whereby ChpC feeds these environmental signals into the Chp system, potentially via PilJ or another MCP, to control twitching motility. PilJ and PilI then modulate T4P surface levels to allow the cell to continue to undergo twitching motility. Our study is the first to link environmental signals to the Chp chemosensory system and refines our understanding of how this system controls twitching motility-mediated biofilm expansion in P. aeruginosa.
Highlights
Pseudomonas aeruginosa is a Gram-negative WHO categorised ‘priority pathogen’due to its high levels of antibiotic resistance and health-care associated infections
In both PAK and PA14, twitching motility-mediated interstitial biofilm expansion was significantly increased in the presence of BSA, mucin and tryptone compared to base media (Figure 1A-B)
In the study we have investigated the twitching motility response of P. aeruginosa to the host-derived signals serum albumin, mucin, and oligopeptides
Summary
Pseudomonas aeruginosa is a Gram-negative WHO categorised ‘priority pathogen’due to its high levels of antibiotic resistance and health-care associated infections. In the lungs of cystic fibrosis (CF) patients this pathogen forms biofilms resulting in chronic lung infections that are the major cause of morbidity and mortality in these individuals [1]. P. aeruginosa is commonly associated with chronic catheter-associated urinary tract infections (CAUTIs) [2]. The success of P. aeruginosa as an opportunistic pathogen is largely attributed to its ability to form biofilms [3] and to produce many cell-associated and secreted virulence factors [4]. Type IV pili (T4P) are a major cell-associated virulence factor which are located at the pole of the cell and are involved in biofilm formation and twitching motility-mediated active biofilm expansion via rounds of extension, surface attachment and retraction [5,6]. Twitching motility is likely to facilitate active biofilm expansion by P
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