RESUMEN
Acinetobacter baumannii is an opportunistic pathogen often found in patients with low immunity. It causes nosocomial infections, which are difficult to treat. This bacterium can rapidly mutate, developing resistance to antimicrobials and adapting to environmental stress, thereby increasing its survival. Understanding such adaptive mechanisms will be beneficial for controlling the spread of A. baumannii. Astrobiology studies have demonstrated that microbiomes from astronauts and manned spaceflight environments show resistance to stress and antibiotics. Astronauts also encounter low immunity during spaceflight missions. The extreme conditions of spaceflight provide a unique research platform for studying how opportunistic pathogens such as A. baumannii adapt to conditions such as microgravity and mutate during spaceflight. In this study, we compared phenotypic variations and analyzed genomic and transcriptomic variations in A. baumannii strains exposed to three different conditions: ST1 (64 days on Tiangong-2 space laboratory), GT1 (ground control), and Aba (original strain). Biofilm formation ability of the ST1 strain increased after 64 days of spaceflight. In addition, high-throughput sequencing revealed that some differentially expressed genes were upregulated in the ST1 strain compared to the GT1 strain. These results provide insights into the environmental adaptation of this widespread pathogen.
Asunto(s)
Acinetobacter baumannii , Vuelo Espacial , Acinetobacter baumannii/genética , Antibacterianos , Biopelículas , China , Genómica , Humanos , TranscriptomaRESUMEN
Streptococcus pneumoniae is one of the most frequent opportunistic pathogens worldwide. DNA processing protein A (DprA) is an important factor involved in bacterial uptake and DNA integration into bacterial genome, but its role in S. pneumoniae virulence remains unclear. The aim of this study was to characterize the effects of the pneumococcal dprA gene on the pathogenesis of S. pneumoniae. To construct a dprA-deficient pneumococcal strain, the dprA gene of the S. pneumoniae strain D39 was inactivated. The virulence of this dprA-deficient strain, designated ΔD39, was compared with that of the wild-type strain by evaluating their respective capabilities to adhere to human pulmonary epithelial cells (PEC-A549) and by analyzing their choline-binding protein expression levels. In addition, the expression profiles of genes associated with virulence and host survival assays were also conducted with the mutant and the wild-type strain. Our results indicate that the capability of ΔD39 to adhere to the PEC-A549 airway cells was significantly lower (p < 0.01) compared with D39. Additionally, the 100-KD choline-binding protein was not detected in ΔD39. The addition of competence-stimulating peptide (CSP) lead to a significantly reduction of psaA mRNA expression in the dprA-deficient mutant and an increased level of psaA transcripts in the wild-type strain (p < 0.01). The median survival time of mice intraperitoneally infected with ΔD39 was significantly higher (p < 0.01) than that of mice infected with D39. The results of this study suggest that DprA has a significant effect on virulence characteristics of S. pneumoniae by influencing the expression of choline-binding protein and PsaA.(AU)
Asunto(s)
Ratas , Streptococcus pneumoniae , Virulencia , Análisis Mutacional de ADN , ADN Bacteriano , Reacción en Cadena en Tiempo Real de la PolimerasaRESUMEN
Abstract Streptococcus pneumoniae is one of the most frequent opportunistic pathogens worldwide. DNA processing protein A (DprA) is an important factor involved in bacterial uptake and DNA integration into bacterial genome, but its role in S. pneumoniae virulence remains unclear. The aim of this study was to characterize the effects of the pneumococcal dprA gene on the pathogenesis of S. pneumoniae. To construct a dprA-deficient pneumococcal strain, the dprA gene of the S. pneumoniae strain D39 was inactivated. The virulence of this dprA-deficient strain, designated ΔD39, was compared with that of the wild-type strain by evaluating their respective capabilities to adhere to human pulmonary epithelial cells (PEC-A549) and by analyzing their choline-binding protein expression levels. In addition, the expression profiles of genes associated with virulence and host survival assays were also conducted with the mutant and the wild-type strain. Our results indicate that the capability of ΔD39 to adhere to the PEC-A549 airway cells was significantly lower (p < 0.01) compared with D39. Additionally, the 100-KD choline-binding protein was not detected in ΔD39. The addition of competence-stimulating peptide (CSP) lead to a significantly reduction of psaA mRNA expression in the dprA-deficient mutant and an increased level of psaA transcripts in the wild-type strain (p < 0.01). The median survival time of mice intraperitoneally infected with ΔD39 was significantly higher (p < 0.01) than that of mice infected with D39. The results of this study suggest that DprA has a significant effect on virulence characteristics of S. pneumoniae by influencing the expression of choline-binding protein and PsaA.
Asunto(s)
Humanos , Animales , Infecciones Neumocócicas/patología , Streptococcus pneumoniae/patogenicidad , Proteínas Bacterianas/metabolismo , Adhesión Bacteriana , Factores de Virulencia/análisis , Proteínas de la Membrana/metabolismo , Infecciones Neumocócicas/microbiología , Streptococcus pneumoniae/genética , Proteínas Bacterianas/análisis , Proteínas Bacterianas/genética , Análisis de Supervivencia , Línea Celular , Factores de Virulencia/genética , Modelos Animales de Enfermedad , Células Epiteliales/microbiología , Técnicas de Inactivación de Genes , Proteínas de la Membrana/genética , RatonesRESUMEN
Streptococcus pneumoniae is one of the most frequent opportunistic pathogens worldwide. DNA processing protein A (DprA) is an important factor involved in bacterial uptake and DNA integration into bacterial genome, but its role in S. pneumoniae virulence remains unclear. The aim of this study was to characterize the effects of the pneumococcal dprA gene on the pathogenesis of S. pneumoniae. To construct a dprA-deficient pneumococcal strain, the dprA gene of the S. pneumoniae strain D39 was inactivated. The virulence of this dprA-deficient strain, designated ΔD39, was compared with that of the wild-type strain by evaluating their respective capabilities to adhere to human pulmonary epithelial cells (PEC-A549) and by analyzing their choline-binding protein expression levels. In addition, the expression profiles of genes associated with virulence and host survival assays were also conducted with the mutant and the wild-type strain. Our results indicate that the capability of ΔD39 to adhere to the PEC-A549 airway cells was significantly lower (p<0.01) compared with D39. Additionally, the 100-KD choline-binding protein was not detected in ΔD39. The addition of competence-stimulating peptide (CSP) lead to a significantly reduction of psaA mRNA expression in the dprA-deficient mutant and an increased level of psaA transcripts in the wild-type strain (p<0.01). The median survival time of mice intraperitoneally infected with ΔD39 was significantly higher (p<0.01) than that of mice infected with D39. The results of this study suggest that DprA has a significant effect on virulence characteristics of S. pneumoniae by influencing the expression of choline-binding protein and PsaA.