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Lutter, E. I.

Publications and source records attributed to Lutter, E. I..

2 recordsLinked to original sources

Differential Metabolite Production Underlies Disruption of the Cystic Fibrosis Airway Microbiota by Pathogens

Cystic fibrosis (CF) is a multisystem disease characterized by the accumulation of mucus in the airways that promotes pathogen colonization, leading to respiratory exacerbations, lung failure, and death. Culture-independent approaches have revealed that the CF airway harbors a complex microbiota, including opportunistic pathogens and bacteria that colonize the oropharynx. Here, we reanalyzed 5,260 16S rRNA gene microbiota datasets to infer ecological associations between members of the CF microbiota. We determined that pathogens are more likely to proliferate and dominate when present, while oropharyngeal bacteria are more likely to form persistent communities. Further, we found higher diversity and increasing numbers of inferred interactions were positively associated with lung function. In contrast, pathogens were negatively associated both with each other and with oropharyngeal bacteria, suggesting that they may disrupt the microbiota. To validate these predictions, we cultured 1,597 bacterial isolates from 96 people with CF and performed 12,542 coculture assays against eight representative CF pathogenic and oropharyngeal bacteria. 23% of these interactions resulted in growth inhibition. While Pseudomonas isolates were, on average, the most inhibitory, we observed variable activity among isolates. We then confirmed that Pseudomonas aeruginosa isolates, even those from the same donor and timepoint, exhibited significant differences in their metabolome and bioactivity profiles that correlated with acquisition of mutations. Together, our results suggest that pathogens may disrupt the CF microbiota and bloom in part through differential metabolite production. Furthermore, these data highlight that characterizing multiple isolates is necessary to capture the full landscape of chemically mediated interactions within microbial communities. ImportanceThe cystic fibrosis (CF) airway harbors a complex microbiota, including oropharyngeal bacteria and opportunistic pathogens that establish chronic infections and cause lung failure. We confirmed that microbiota diversity is correlated with health and that a pathogen-dominated microbiota is associated with reduced lung function. We then inferred microbial interactions, which suggested that pathogens are able to disrupt the microbiota. To validate these predictions, we cultured bacterial isolates from people with CF and performed thousands of coculture assays, finding that approximately one-quarter of interactions resulted in growth inhibition. Pseudomonas broadly inhibited other members of the CF airway microbiota. However, we observed marked variability in bioactivity and metabolite profiles of Pseudomonas aeruginosa isolates, even from the same donor at the same time. Our results suggest that pathogens disrupt the CF microbiota, possibly through bioactive metabolite production, and that characterizing multiple isolates is necessary to capture the complete picture of interactions in these communities.

microbiology↗

EF-Hand Calcium Sensor, EfhP, Controls Transcriptional Regulation of Iron Uptake by Calcium in Pseudomonas aeruginosa

The human pathogen Pseudomonas aeruginosa poses a major risk for a range of severe infections, particularly lung infections in patients suffering from cystic fibrosis (CF). As previously reported, the virulent behavior of this pathogen is enhanced by elevated levels of Ca2+ that are commonly present in CF nasal and lung fluids. In addition, a Ca2+-binding EF-hand protein, EfhP (PA4107), was partially characterized and shown to be critical for the Ca2+-regulated virulence in P. aeruginosa. Here we describe the rapid (10 min, 60 min), and adaptive (12 h) transcriptional responses of PAO1 to elevated Ca2+ detected by genome-wide RNA sequencing and show that efhP deletion significantly hindered both rapid and adaptive Ca2+ regulation. The most differentially regulated genes included multiple Fe sequestering mechanisms, a large number of extracytoplasmic function sigma factors (ECF{sigma}) and several virulence factors, such as production of pyocins. The Ca2+ regulation of Fe uptake was also observed in CF clinical isolates and appeared to involve the global regulator Fur. In addition, we showed that the efhP transcription is controlled by Ca2+ and Fe, and this regulation required Ca2+-dependent two-component regulatory system CarSR. Furthermore, the efhP expression is significantly increased in CF clinical isolates and upon pathogen internalization into epithelial cells. Overall, the results established for the first time that Ca2+ controls Fe sequestering mechanisms in P. aeruginosa and that EfhP plays a key role in the regulatory interconnectedness between Ca2+ and Fe signaling pathways, the two distinct and important signaling pathways that guide the pathogens adaptation to host. IMPORTANCEPseudomonas aeruginosa (Pa) poses a major risk for severe infections, particularly in patients suffering from cystic fibrosis (CF). For the first time, kinetic RNA sequencing analysis identified Pa rapid and adaptive transcriptional responses to Ca2+ levels consistent with those present in CF respiratory fluids. The most highly upregulated processes include iron sequestering, iron starvation sigma factors, and self-lysis factors pyocins. An EF-hand Ca2+ sensor, EfhP, is required for at least 1/3 of the Ca2+ response, including all the iron uptake mechanisms and production of pyocins. Transcription of efhP itself is regulated by Ca2+, Fe, and increases during interactions with host epithelial cells, suggesting the proteins important role in Pa infections. The findings establish the regulatory interconnectedness between Ca2+ and iron signaling pathways that shape Pa transcriptional responses. Therefore, understanding Pas transcriptional response to Ca2+ and associated regulatory mechanisms will serve the development of future therapeutics targeting Pa dangerous infections.

microbiology↗