Polymicrobial Communities Research Articles

Impact of carbon sources in airport de-icing compounds on the growth of Sphaerotilus natans

Airport de-icing has been linked with the growth of undesirable river biofilms (URBs, formerly “sewage fungus”), a manifestation of organic pollution causing long-term ecological damage to watercourses. URBs are a polymicrobial community, with one key taxon standing out in literature: Sphaerotilus natans, a filamentous bacterium also found in sewage treatment and activated sludges. An industry often implicated in causing URBs is airport de-icing, with large biofilms often developing downstream of airport discharges in winter months. However, it is not yet clear which de-icers may cause URBs and how they influence growth. Therefore, specific objectives were to (i) determine which freeze-point depressants (FPDs) can be utilized by S. natans; (ii) examine differences in the growth kinetics between FPDs; and (iii) compare pure-FPDs to commercial airport de-icers (CADs) as carbon sources, to determine impacts of additives. This study employed a turbidimetric micro-batch culture design to conduct microbial growth experiments, using S. natans and a minimal medium supplemented with airport de-icer as the carbon source. Equimolar carbon concentrations were used to compare the effects of common FPDs and CADs – each containing a specific FPD. Growth was assessed via optical density (OD600) measurements, from which time-to-detection, maximum rate of change, and maximum optical density were derived and kinetics inferred. S. natans was found to grow effectively on all FPDs tested, although the microbial yield was heavily dependent on the carbon concentration for all FPDs and CADs. Sodium acetate generated the quickest growth, with the lowest TTD (lag-time) for all but the lowest concentrations tested. Propylene glycol produced the greatest maxOD (total growth), whereas ethylene glycol had a higher limiting concentration for maxROC (growth rate). The mixture of compounds and additives in commercial products did not significantly impact the growth of S. natans. This research provides evidence from controlled laboratory experiments that airport de-icers support the growth of S. natans. The differences in growth kinetics observed for the FPDs and CADs could inform improved mitigation or treatment to reduce the incidence and ecological impacts of URBs.

A novel PhoPQ-potentiated mechanism of colistin resistance impairs membrane integrity in Pseudomonas aeruginosa.

Polymicrobial communities are often recalcitrant to antibiotic treatment because interactions between different microbes can dramatically alter their responses and susceptibility to antimicrobials. However, the mechanisms of evolving antimicrobial resistance in such polymicrobial environments are poorly understood. We previously reported that Mg 2+ depletion caused by the fungus Candida albicans can enable Pseudomonas aeruginosa to acquire significant resistance to colistin, a last-resort antibiotic targeting bacterial membrane. Here, we dissect the genetic and biochemical basis of this increased colistin resistance. We show that P. aeruginosa cells can acquire colistin resistance using three distinct evolutionary trajectories involving mutations in genes involved in lipid A biosynthesis, lipid A modifications that are dependent on low Mg 2+ , and a putative Mg 2+ transporter, PA4824. These mutations confer colistin resistance by altering acyl chains, hydroxylation, and aminoarabinose modification of lipid A moieties on the bacterial outer membrane. In all cases, enhanced colistin resistance initially depends on the low Mg 2+ -responsive PhoPQ pathway, which potentiates the evolution of resistance mutations and lipid A modifications that do not occur without Mg 2+ depletion. However, the PhoPQ pathway is not required to maintain high colistin resistance in all cases. In most cases, the genetic and biochemical changes associated with these novel forms of colistin resistance also impair bacterial membrane integrity, leading to fitness costs. Our findings provide molecular insights into how nutritional competition drives a novel antibiotic resistance mechanism and its ensuing fitness tradeoffs.

Swarming bacteria exhibit developmental phase transitions to establish scattered colonies in new regions.

The bacterial Type 9 Secretion System (T9SS) is essential for the development of periodontal diseases and Bacteroidetes gliding motility. T9SS-driven motile bacteria, abundant within the human oral microbiota, transport non-motile oral microbes and bacteriophages as cargo, shaping the spatial structure of polymicrobial communities. However, the physical rules governing the dispersal of T9SS-driven bacterial swarms are barely understood. Here, we collected time-lapse images, under anaerobic conditions, of developing swarms of a T9SS-driven microbe common to the human oral microbiota. Tracking of swarms revealed that small peripheral flares emerging from a colony develop structures that resemble fireworks displaying a chrysanthemum effect and flower-like patterns that convert to wave-like patterns and which further evolve into scattered microcolonies. Particle-image velocimetry showed density-dependent phase transitions and initial vorticity within these emerging patterns. Numerical simulations demonstrate that these patterns arise due to changes in swarm speed and alignment strength. Our data reveal a strategy used by an anaerobic swarming bacterium to control swarm behavior, resulting in scattered microcolonies distant from the mother colony, thus reducing competition for resources among colony members. This might ensure species survival even if conditions change drastically in one location of the human oral cavity.

Assessing peri-implant bacterial community structure: the effect of microbiome sample collection method

BackgroundOral microbiota comprises polymicrobial communities shaped by mutualistic coevolution with the host, contributing to homeostasis and regulating immune function. Nevertheless, dysbiosis of oral bacterial communities is associated with a number of clinical symptoms that ranges from infections to oral cancer. Peri-implant diseases are biofilm-associated inflammatory conditions affecting the soft and hard tissues around dental implants. Characterization and identification of the biofilm community are essential for the understanding of the pathophysiology of such diseases. For that sampling methods should be representative of the biofilm communities Therefore, there is a need to know the effect of different sampling strategies on the biofilm characterization by next generation sequencing.MethodsWith the aim of selecting an appropriate microbiome sampling procedure for periimplant biofilms, next generation sequencing was used for characterizing the bacterial communities obtained by three different sampling strategies two months after transepithelial abutment placement: adjacent periodontal crevicular fluid (ToCF), crevicular fluid from transepithelial abutment (TACF) and transepithelial abutment (TA).ResultsSignificant differences in multiple alpha diversity indices were detected at both the OTU and the genus level between different sampling procedures. Differentially abundant taxa were detected between sample collection strategies, including peri-implant health and disease related taxa. At the community level significant differences were also detected between TACF and TA and also between TA and ToCF. Moreover, differential network properties and association patterns were identified.ConclusionsThe selection of sample collection strategy can significantly affect the community composition and structure.Trial registrationThis research is part of a randomized clinical trial that was designed to assess the effect of transepithelial abutment surface on the biofilm formation. The trial was registered at Trial Registration ClinicalTrials.gov under the number NCT03554876.

A crayfish chitosan-based bioactive film to treat vaginal infections: A sustainable approach

Polymicrobial communities are seen to be a sign of health, but they can turn detrimental when an excess of pathogenic species leads to recurring vaginal infections. This microbiological imbalance may decrease women's fertility, increasing also the risk of infection by Human Papillomavirus (HPV) and/or other sexually transmitted infections (STIs). There is a worldwide need for smart/sustainable solutions to tackle these types of infections. Hereupon, we investigated, as a potential solution, the use of crayfish chitosan-based membrane as a mucoadhesive, antimicrobial, biocompatible and biodegradable material. Chitosan was chemically extracted with a process yield of ca. 63 % and a degree of deacetylation of ca. 65 %. Further chitosan was characterized by FTIR, DSC, XRD and zeta potential. Antimicrobial and antioxidant activities were tested by microbicide concentration and ABTS methods. The extracted chitosan was confirmed to be antioxidant and antimicrobial against Escherichia coli, Candida albicans, Staphylococcus aureus (methicillin resistant and susceptible strains). Vaginal films using chitosan extracted from crayfish shells were produced by solvent casting, and the biological profile was tested in simulated vaginal fluid as a proof of concept. The main data showed that the vaginal films prepared were active against several microorganisms responsible for vaginal infections, demonstrating their potential in the field.

Convergent evolution in toxin detection and resistance provides evidence for conserved bacterial–fungal interactions

Microbes rarely exist in isolation and instead form complex polymicrobial communities. As a result, microbes have developed intricate offensive and defensive strategies that enhance their fitness in these complex communities. Thus, identifying and understanding the molecular mechanisms controlling polymicrobial interactions is critical for understanding the function of microbial communities. In this study, we show that the gram-negative opportunistic human pathogen Pseudomonas aeruginosa, which frequently causes infection alongside a plethora of other microbes including fungi, encodes a genetic network which can detect and defend against gliotoxin, a potent, disulfide-containing antimicrobial produced by the ubiquitous filamentous fungus Aspergillus fumigatus. We show that gliotoxin exposure disrupts P. aeruginosa zinc homeostasis, leading to transcriptional activation of a gene encoding a previously uncharacterized dithiol oxidase (herein named as DnoP), which detoxifies gliotoxin and structurally related toxins. Despite sharing little homology to the A. fumigatus gliotoxin resistance protein (GliT), the enzymatic mechanism of DnoP from P. aeruginosa appears to be identical that used by A. fumigatus. Thus, DnoP and its transcriptional induction by low zinc represent a rare example of both convergent evolution of toxin defense and environmental cue sensing across kingdoms. Collectively, these data provide compelling evidence that P. aeruginosa has evolved to survive exposure to an A. fumigatus disulfide-containing toxin in the natural environment.

Community context influences the conjugation efficiency of Escherichia coli.

In urinary tract infections (UTIs), different bacteria can live in a polymicrobial community consisting of different species. It is unknown how community members affect the conjugation efficiency of uropathogenic Escherichia coli. We investigated the influence of individual species often coisolated from urinary infections (UTI) on the conjugation efficiency of E. coli isolates in artificial urine medium. Pairwise conjugation rate experiments were conducted between a donor E. coli strain containing the pOXA-48 plasmid and six uropathogenic E. coli isolates, in the presence and absence of five different species commonly coisolated in polymicrobial UTIs to elucidate their effect on the conjugation efficiency of E. coli. We found that the basal conjugation rates of pOXA-48, in the absence of other species, are dependent on the bacterial host genetic background. Additionally, we found that bacterial interactions have an overall positive effect on the conjugation rate of pOXA-48. Particularly, Gram-positive enterococcal species were found to enhance the conjugation rates towards uropathogenic E. coli isolates. We hypothesize that the nature of the coculture and physical interactions are important for these increased conjugation rates in an artificial urine medium environment.

Dpr-mediated H2O2 resistance contributes to streptococcus survival in a cystic fibrosis airway model system.

Streptococcus spp. are recognized as a highly prevalent pathogen in cystic fibrosis (CF) airway infections. However, the role of this microbe in clinical outcomes for persons with CF is poorly understood. Here, we leverage a polymicrobial community system previously developed by our group to model CF airway infections as a tool to investigate a Pseudomonas-Streptococcus interaction involving reactive oxygen species (ROS). We show that protection against ROS is required for Streptococcus sanguinis survival in a clinically relevant polymicrobial system. Using this model system to study interspecies interactions contributes to our broader understanding of the complex role of Streptococcus spp. in the CF lung.

Widespread fungal-bacterial competition for magnesium lowers bacterial susceptibility to polymyxin antibiotics.

Fungi and bacteria coexist in many polymicrobial communities, yet the molecular basis of their interactions remains poorly understood. Here, we show that the fungus Candida albicans sequesters essential magnesium ions from the bacterium Pseudomonas aeruginosa. To counteract fungal Mg2+ sequestration, P. aeruginosa expresses the Mg2+ transporter MgtA when Mg2+ levels are low. Thus, loss of MgtA specifically impairs P. aeruginosa in co-culture with C. albicans, but fitness can be restored by supplementing Mg2+. Using a panel of fungi and bacteria, we show that Mg2+ sequestration is a general mechanism of fungal antagonism against gram-negative bacteria. Mg2+ limitation enhances bacterial resistance to polymyxin antibiotics like colistin, which target gram-negative bacterial membranes. Indeed, experimental evolution reveals that P. aeruginosa evolves C. albicans-dependent colistin resistance via non-canonical means; antifungal treatment renders resistant bacteria colistin-sensitive. Our work suggests that fungal-bacterial competition could profoundly impact polymicrobial infection treatment with antibiotics of last resort.

Commensal E. coli limits Salmonella gut invasion during inflammation by producing toxin-bound siderophores in a tonB-dependent manner.

The gastrointestinal tract is densely colonized by a polymicrobial community known as the microbiota which serves as primary line of defence against pathogen invasion. The microbiota can limit gut-luminal pathogen growth at different stages of infection. This can be traced to specific commensal strains exhibiting direct or indirect protective functions. Although these mechanisms hold the potential to develop new approaches to combat enteric pathogens, they remain far from being completely described. In this study, we investigated how a mouse commensal Escherichia coli can outcompete Salmonella enterica serovar Typhimurium (S. Tm). Using a salmonellosis mouse model, we found that the commensal E. coli 8178 strain relies on a trojan horse trap strategy to limit S. Tm expansion in the inflamed gut. Combining mutants and reporter tools, we demonstrated that inflammation triggers the expression of the E. coli 8178 antimicrobial microcin H47 toxin which, when fused to salmochelin siderophores, can specifically alter S. Tm growth. This protective function was compromised upon disruption of the E. coli 8178 tonB-dependent catecholate siderophore uptake system, highlighting a previously unappreciated crosstalk between iron intake and microcin H47 activity. By identifying the genetic determinants mediating S. Tm competition, our work not only provides a better mechanistic understanding of the protective function displayed by members of the gut microbiota but also further expands the general contribution of microcins in bacterial antagonistic relationships. Ultimately, such insights can open new avenues for developing microbiota-based approaches to better control intestinal infections.

Influence of β-lactam pharmacodynamics on the systems microbiology of gram-positive and gram-negative polymicrobial communities.

We sought to evaluate the pharmacodynamics of β-lactam antibacterials against polymicrobial communities of clinically relevant gram-positive and gram-negative pathogens. Two Enterococcus faecalis isolates, two Staphylococcus aureus isolates, and three Escherichia coli isolates with varying β-lactamase production were evaluated in static time-killing experiments. Each gram-positive isolate was exposed to a concentration array of ampicillin (E. faecalis) or cefazolin (S. aureus) alone and during co-culture with an E. coli isolate that was β-lactamase-deficient, produced TEM-1, or produced KPC-3/TEM-1B. The results of the time-killing experiments were summarized using an integrated pharmacokinetic/pharmacodynamics analysis as well as mathematical modelling to fully characterize the antibacterial pharmacodynamics. In the integrated analysis, the maximum killing of ampicillin (Emax) against both E. faecalis isolates was ≥ 4.11 during monoculture experiments or co-culture with β-lactamase-deficient E. coli, whereas the Emax was reduced to ≤ 1.54 during co-culture with β-lactamase-producing E. coli. In comparison to monoculture experiments, culturing S. aureus with KPC-producing E. coli resulted in reductions of the cefazolin Emax from 3.25 and 3.71 down to 2.02 and 2.98, respectively. Two mathematical models were created to describe the interactions between E. coli and either E. faecalis or S. aureus. When in co-culture with E. coli, S. aureus experienced a reduction in its cefazolin Kmax by 24.8% (23.1%RSE). Similarly, β-lactamase-producing E. coli preferentially protected the ampicillin-resistant E. faecalis subpopulation, reducing Kmax,r by 90.1% (14%RSE). β-lactamase-producing E. coli were capable of protecting S. aureus and E. faecalis from exposure to β-lactam antibacterials.

The polymicrobial pathogenicity of Porphyromonas gingivalis.

Accumulating microbiome data and mechanistic studies in vitro and in vivo have refined our understanding of the oral microbiota as a functionally integrated polymicrobial community. Emergent properties of these communities are driven to a large extent by interspecies communication which can be based on physical association, secreted small molecules or nutritional exchange. Porphyromonas gingivalis is a consensus periodontal pathogen; however, virulence is only expressed in the context of a polymicrobial community. Multivalent fimbriae mediate attachment to other oral species which can initiate a distinct transcriptional program in both constituents of the binding pair. P. gingivalis also responds to small molecules and nutritional cues produced by partner organisms. Physiological interdependence forms the basis of complex networks of cooperating organisms which begin to resemble an organismal entity exhibiting a spectrum of pathogenic potential.

Triple threat: how diabetes results in worsened bacterial infections.

Diabetes mellitus, characterized by impaired insulin signaling, is associated with increased incidence and severity of infections. Various diabetes-related complications contribute to exacerbated bacterial infections, including hyperglycemia, innate immune cell dysfunction, and infection with antibiotic-resistant bacterial strains. One defining symptom of diabetes is hyperglycemia, resulting in elevated blood and tissue glucose concentrations. Glucose is the preferred carbon source of several bacterial pathogens, and hyperglycemia escalates bacterial growth and virulence. Hyperglycemia promotes specific mechanisms of bacterial virulence known to contribute to infection chronicity, including tissue adherence and biofilm formation. Foot infections are a significant source of morbidity in individuals with diabetes and consist of biofilm-associated polymicrobial communities. Bacteria perform complex interspecies behaviors conducive to their growth and virulence within biofilms, including metabolic cross-feeding and altered phenotypes more tolerant to antibiotic therapeutics. Moreover, the metabolic dysfunction caused by diabetes compromises immune cell function, resulting in immune suppression. Impaired insulin signaling induces aberrations in phagocytic cells, which are crucial mediators for controlling and resolving bacterial infections. These aberrancies encompass altered cytokine profiles, the migratory and chemotactic mechanisms of neutrophils, and the metabolic reprogramming required for the oxidative burst and subsequent generation of bactericidal free radicals. Furthermore, the immune suppression caused by diabetes and the polymicrobial nature of the diabetic infection microenvironment may promote the emergence of novel strains of multidrug-resistant bacterial pathogens. This review focuses on the "triple threat" linked to worsened bacterial infections in individuals with diabetes: (i) altered nutritional availability in diabetic tissues, (ii) diabetes-associated immune suppression, and (iii) antibiotic treatment failure.

Competition quenching strategies reduce antibiotic tolerance in polymicrobial biofilms

Bacteria typically live in dense communities where they are surrounded by other species and compete for a limited amount of resources. These competitive interactions can induce defensive responses that also protect against antimicrobials, potentially complicating the antimicrobial treatment of pathogens residing in polymicrobial consortia. Therefore, we evaluate the potential of alternative antivirulence strategies that quench this response to competition. We test three competition quenching approaches: (i) interference with the attack mechanism of surrounding competitors, (ii) inhibition of the stress response systems that detect competition, and (iii) reduction of the overall level of competition in the community by lowering the population density. We show that either strategy can prevent the induction of antimicrobial tolerance of Salmonella Typhimurium in response to competitors. Competition quenching strategies can thus reduce tolerance of pathogens residing in polymicrobial communities and could contribute to the improved eradication of these pathogens via traditional methods.

Staphopain mediated virulence and antibiotic resistance alteration in co-infection of Staphylococcus aureus and Pseudomonas aeruginosa: an animal model

Polymicrobial communities lead to worsen the wound infections, due to mixed biofilms, increased antibiotic resistance, and altered virulence production. Promising approaches, including enzymes, may overcome the complicated condition of polymicrobial infections. Therefore, this study aimed to investigate Staphopain A-mediated virulence and resistance alteration in an animal model of Staphylococcus aureus and Pseudomonas aeruginosa co-infection. S. aureus and P. aeruginosa were co-cultured on the L-929 cell line and wound infection in an animal model. Then, recombinant staphopain A was purified and used to treat mono- and co-infections. Following the treatment, changes in virulence factors and resistance were investigated through phenotypic methods and RT-PCR. Staphopain A resulted in a notable reduction in the viability of S. aureus and P. aeruginosa. The biofilm formed in the wound infection in both animal model and cell culture was disrupted remarkably. Moreover, the biofilm-encoding genes, quorum sensing regulating genes, and virulence factors (hemolysin and pyocyanin) controlled by QS were down-regulated in both microorganisms. Furthermore, the resistance to vancomycin and doripenem decreased following treatment with staphopain A. According to this study, staphopain A might promote wound healing and cure co-infection. It seems to be a promising agent to combine with antibiotics to overcome hard-to-cure infections.

Siderophores promote cooperative interspecies and intraspecies cross-protection against antibiotics in vitro.

The antibiotic cefiderocol hijacks iron transporters to facilitate its uptake and resists β-lactamase degradation. While effective, resistance has been detected clinically with unknown mechanisms. Here, using experimental evolution, we identified cefiderocol resistance mutations in Pseudomonas aeruginosa. Resistance was multifactorial in host-mimicking growth media, led to multidrug resistance and paid fitness costs in cefiderocol-free environments. However, kin selection drove some resistant populations to cross-protect susceptible individuals from killing by increasing pyoverdine secretion via a two-component sensor mutation. While pyochelin sensitized P. aeruginosa to cefiderocol killing, pyoverdine and the enterobacteria siderophore enterobactin displaced iron from cefiderocol, preventing uptake by susceptible cells. Among 113 P. aeruginosa intensive care unit clinical isolates, pyoverdine production directly correlated with cefiderocol tolerance, and high pyoverdine producing isolates cross-protected susceptible P. aeruginosa and other Gram-negative bacteria. These in vitro data show that antibiotic cross-protection can occur via degradation-independent mechanisms and siderophores can serve unexpected protective cooperative roles in polymicrobial communities.

Sputum metagenomics of people with bronchiectasis.

The microbiota in the sputum of people with bronchiectasis has repeatedly been investigated in cohorts of different geographic origin, but so far has not been studied to the species level in comparison to control populations including healthy adults and smokers without lung disease. The microbial metagenome from sputa of 101 European Bronchiectasis Registry (EMBARC) study participants was examined by using whole-genome shotgun sequencing. Our analysis of the metagenome of people with bronchiectasis revealed four clusters characterised by a predominance of Haemophilus influenzae, Pseudomonas aeruginosa or polymicrobial communities with varying compositions of nonpathogenic commensals and opportunistic pathogens. The metagenomes of the severely affected patients showed individual profiles characterised by low alpha diversity. Importantly, nearly 50% of patients with severe disease were grouped in a cluster characterised by commensals. Comparisons with the sputum metagenomes of healthy smokers and healthy nonsmokers revealed a gradient of depletion of taxa in bronchiectasis, most often Neisseria subflava, Fusobacterium periodonticum and Eubacterium sulci. The gradient of depletion of commensal taxa found in healthy airways is a key feature of bronchiectasis associated with disease severity.

The Microbiological Landscape of Diabetic Foot Infections: Implications for Treatment and Prevention

Diabetic foot infections (DFIs) represent one of the most serious and frequent complications resulting from diabetes mellitus, causing substantial morbidity as well as enhanced risk for amputation. The microbiological world of DIFs is typically multifaceted and usually includes a polymicrobial community with both aerobic bacteria this anaerobe the purpose of this review is to decompose the current knowledge about microbial diversity in DFIs, their resistance patterns and biofilms contribution for resilience towards infection persistence and therapy. Development of molecular techniques has allowed increased insight into the DFI microbiome, not only uncovering prevalent pathogens such as Staphylococcus aureus and Pseudomonas aeruginosa but also lesser frequently isolated organisms. The employment of multidrug-resistant organisms and the intricate relationship between microbial species within biofilms present serious management challenges. The review focuses on the relevance of early and accurate diagnosis using culture-based methodologies as well molecular methods that, in turn, would enable more specific antimicrobial therapy. Moreover, the opportunity of new antibacterial agents will be available; other local delivery systems and adjunctive therapies like negative pressure wound therapy would also be addressed. Strategies of prevention that involve patient education, regular foot checks and proper glycemic control form part of essential measures in reducing incidences of DFIs. An interdisciplinary approach to care is highlighted in the review, influencing diabetology specialists, infectious disease physicians and microbiologists as well as podiatrists be able to improve treatment outcomes. This review aims to provide the most recent synthesis on microbiological aspects of DFIs and their clinical implications, with an intent of informing development of more effective strategies for management thus improving patient’s quality life as well reducing pressure from health care systems.

The type IV pilus chemoreceptor PilJ controls chemotaxis of one bacterial species towards another.

Bacteria live in social communities, where the ability to sense and respond to interspecies and environmental signals is critical for survival. We previously showed the pathogen Pseudomonas aeruginosa detects secreted peptides from bacterial competitors and navigates through interspecies signal gradients using pilus-based motility. Yet, it was unknown whether P. aeruginosa utilizes a designated chemosensory system for this behavior. Here, we performed a systematic genetic analysis of a putative pilus chemosensory system, followed by high-speed live-imaging and single-cell tracking, to reveal behaviors of mutants that retain motility but are blind to interspecies signals. The enzymes predicted to methylate (PilK) and demethylate (ChpB) the putative pilus chemoreceptor, PilJ, are necessary for cells to control the direction of migration. While these findings implicate PilJ as a bona fide chemoreceptor, such function had yet to be experimentally defined, as full-length PilJ is essential for motility. Thus, we constructed systematic genetic modifications of PilJ and found that without the predicted ligand binding domains or predicted methylation sites, cells lose the ability to detect competitor gradients, despite retaining pilus-mediated motility. Chemotaxis trajectory analysis revealed that increased probability and size of P. aeruginosa pilus-mediated steps towards S. aureus peptides, versus steps away, determines motility bias in wild type cells. However, PilJ mutants blind to interspecies signals take less frequent steps towards S. aureus or steps of equal size towards and away. Collectively, this work uncovers the chemosensory nature of PilJ, provides insight into how cell movements are biased during pilus-based chemotaxis, and identifies chemotactic interactions necessary for bacterial survival in polymicrobial communities, revealing putative pathways where therapeutic intervention might disrupt bacterial communication.

Autolysis of Pseudomonas aeruginosa Quorum-Sensing Mutant Is Suppressed by Staphylococcus aureus through Iron-Dependent Metabolism.

Microorganisms usually coexist as a multifaceted polymicrobial community in the natural habitats and at mucosal sites of the human body. Two opportunistic human pathogens, Pseudomonas aeruginosa and Staphylococcus aureus commonly coexist in the bacterial infections for hospitalized and/or immunocompromised patients. Here, we observed that autolysis of the P. aeruginosa quorum-sensing (QS) mutant (lasRmvfR) was suppressed by the presence of the S. aureus cells in vitro. The QS mutant still displayed killing against S. aureus cells, suggesting the link between the S. aureus-killing activity and the autolysis suppression. Independent screens of the P. aeruginosa transposon mutants defective in the S. aureus-killing and the S. aureus transposon mutants devoid of the autolysis suppression revealed the genetic link between both phenotypes, suggesting that the iron-dependent metabolism involving S. aureus exoproteins might be central to both phenotypes. The autolysis was suppressed by iron treatment as well. These results suggest that the interaction between P. aeruginosa and S. aureus might be governed by mechanisms that necessitate the QS circuitry as well as the metabolism involving the extracellular iron resources during the polymicrobial infections in the human airway.